Animal Nutrition - Small and Large Animals at WCVM

VLAC 211 Animal Nutrition

Objectives: An understanding of basic nutrition concepts and terminology Relationship between nutrition and animal function Sources of information Examples of nutrition application

Outline

Classification of nutrients and nutrient analysis Feed classification and composition Digestibility: measurement and variability Energy requirement and feed energy utilization Water as a nutrient and water quality Carbohydrates Lipids Protein: monogastric animals and ruminants Minerals: macro and micro Vitamins: fat and water soluble

References:

Basic Animal Nutrition and Feeding. Pond, Church and Pond, John Wiley, Fourth Edition 1995.

Applied Animal Nutrition; Feeds and Feeding. Cheeke, Collier MacMillan, 2nd Ed, 1999.

Nutrient Requirements of Domestic Animals. National Academy of Sciences, National Research Council (NAS-NRC), Washington, D.C.

Description graduate veterinarian requirement: Veterinary Nutrition Education Program AVMA (www.acvn.org)

On-line Glossaries: Definitions of English terms in Animal Science and Agriculture USA: http://www.epa.gov/agriculture/ag101/glossary.htmlCanada: http://www.aps.uoguelph.ca/~gking/Ag_2350/glossary.htm

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http://www.aps.uoguelph.ca/~gking/Ag_2350/glossary.htm

http://www.epa.gov/agriculture/ag101/glossary.html

What to learn from Nutrition Lectures?

How feeds are classified Differences in composition How types of feeds differ

Digestibility concepts and influencing factors Energy partition in the animal and feed energy GE to NE Energy requirement estimation Carbohydrates as energy and gut microbe modifiers Lipids as energy and fatty acid sources Monogastric animal protein nutrition, essential amino acids, protein quality Ruminant protein utilization, rumen microbial protein, bypass protein, Cornell fractions Under what circumstances may macro and micro mineral deficiencies occur, general

signs of deficiencies, appropriate supplements Be familiar with fat and water soluble vitamins Basic nutrition vocabulary and understanding of nutrition principles

Laboratories outcomes

Be familiar with feedstuffs and simple methods of ration formulation Sensitivity to the possibility of inadequate nutrition or toxicity of diet constituents in all

clinical cases Understand general ration characteristics, digestibility / availability, nutrient requirements

and approaches to determining requirements Some familiarity with feed processing and equipment

Nutrition is anInterdisciplinary Science

It involves the following science disciplines: Digestive physiology Biochemistry Analytical chemistry Endocrinology and Metabolism Microbiology Pathology Nutritional Genomics and Genetics Animal behaviour and management Environmental studies Economic Studies

Animal Nutrition also incorporates economic considerations

NUTRIENT:

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Samantha Lynn Bray, 10/24/16,

How animals use energy


We take important aspects of various subjects to achieve optimal nutrition for an animal.


How does diet influence the microbiome of the gut.

Any chemical element or compound in the diet that supports life processes, such as reproduction, growth, lactation, draft power, and maintenance.

Classes of nutrients:1. Water2. Proteins and amino acids3. Carbohydrates4. Lipids5. Vitamins6. Inorganic Elements (Minerals)

*Note energy is not considered a nutrient – it is derived from nutrients: lipids, carbohydrates and protein

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Are protein/amino acids good sources of energy? NO – protein is not desireable in terms of use for energy (it is expensive). Protein breakdown also results in production of urea – which must be metabolized in the kidneys for excretion in urea (energy extensive process) Fat/Carbohydrates are a lot cheaper and are preferred as an energy source


Contains carbon that can be oxidized (burned) for energy.


Starch and Fiber


CLASSIC EXAM QUESTION: What are the main classes of nutrients.

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Animals can survive on non-protein nitrogen – microbes can use these non-protein nitrogen and convert into microbial protein (of high quality).


Know the main groups: nitrogen containing (protein ( A.A/non-protein ( nitrate, amines, etc). Lipids – fatty acids, sterols, phospholipids, FFA. Carbohydrates – polysaccharides, monosaccharides, disaccharides, fibrous Vitamins – water or fat soluble Essential Elements – macro/micro elements Possible Essential Non Essential Toxic

Specialty terms:

Functional foods or nutraceuticals: These are foods that have non-nutrient effects that contribute to health

Pre- and pro-biotics:Prebiotics are nutrients that specifically allow growth of beneficial microbial populations in the gut

Probiotics: are microbial communities/strains included in feed (inoculation) to colonize the gut and improve gut health of the host

When fiber is added to water it forms a gel – this happens in the gut and then the microbes go and aggregate on it.

Energy: Not a nutrient initself but fuel (ATP) provided by lipid, carbohydrate, and carbon skeleton of amino acids after removal of N.

Essential Nutrient: Required in diet because it cannot be synthesized by the body in sufficient amounts to satisfy metabolic needs.

Nutrition:

Purpose of Nutrition is to provide Nourishment

It is the science (or study) of daily diet and health

1. Nutrient requirements of animals

2. Content of nutrients in food or feed

3. The balancing (mixing in specific amounts) of a mixture of feed ingredients to meet the animal’s nutrient requirement at lowest cost

4. Through computer models predict from feed nutrient content the actual animal performance that one can expect from an animal fed a certain diet.

What makes a good diet?

Must contain all the essential nutrients

And in the correct amounts and proportions

Must be palatable (taste good)

Cost - must be economical

Must be safe – no toxic substances

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Applies to farm animals ( that get turned into meat for human consumption. Cat and dog food production – not as stringent because these animals are not going to be turned into food.


What properties will enhance GI health. Less susceptibility to colon cancer Growth of beneficial microbes


Helps you figure out the ratios that you need to meet the requirements of a particular species/diet.


What is the nutrient requirement of this certain animal in a specific life stage. Is it a meat animal, pregnant, lactating, etc.


Carnivores have different protein requirement than dogs. This is a result of adaptation and natural selection.


VOLATILE FATTY ACIDS – C2 (acetic), C3 (propionic acid), C4 (butyric acid – stimulates growth of epithelial in the gut and protects against colon cancer). Fiber fermented by microbes into VFAs.


Fiber source – vegetables (turnip/carrots) – gives them functional fiber that is INTACT and can go to the gut and stimulate the biome. We grind up fiber to make it more digestible


Wheat bran – is good but when it is ground up it has less fiber


Probiotics might be most useful in the early developmental stages.


Very little probiotics used in animal nutrition (livestock) – is driven by economy. If you say probiotics will increase weight of pigs of viability of piglets – no hard data to show this – livestock industry is reluctant to use these supplements because there is not a lot of scientific data.


Biggest challenge – how to get anaerobic probiotics into food without killing the microbe.


Very common now and days – found in yogurt.


Basically try to inoculate the GI tract with microbes (lactic acid bacteria) that promote a healthy gut environment.


Feed the microbe population in the gut – oligosaccharides – very good for stimulating lactic acid producing bacteria. Prebiotics are not culture – they are just nutrients for the microbes.


Fiber content of diet is important – can stimulate microbiome/hindgut fermentation – reduces the risk of colon cancer in humans.


The value of the food (not in terms of nutrient content) more about physical effect of food in the digestive track of animals/people.

Must meet functional food requirements as well. The Application of Nutrition in Feeding Animals (How to approach feeding management in steps):

1. Question: What is the nutrient requirement of class of animal for specific productive or physiological function? (look this up in tables)

Note that these are minimum requirements for typically healthy animals under ideal conditions (thus not very practical)

They do not take into consideration stress, disease or parasite conditions of the animal

Feed formulation must also be sensitive to environmental considerations (low N and P in urine and feces)

Requirement vs allowance Requirement is the minimum; allowance is a practical approach allowing for variabilityDogs: Requirements (NRC 2006)Allowance/practical applications AAFCO (2007)

2. Question: What is the nutrient content of feed ingredients?

Preferably from chemical analysis, Near Infrared Spectroscopy (NIR) or else from tables and data bases; and

a. Consider availability of nutrients (digestibility)b. Consider anti-nutritional factorsc. Consider antagonism between nutrients and other factors (feed matrix)

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Especially important in mineral nutrition – is quite effected by other factors in the feed mix.


In soybean there is trypsin inhibitor (a protein needed for protein digestion). Causes a very poor AA availability. Brief heat treatment of the trypsin inhibitor will inhibit the inhibitor.


Can tell you that the food has 60% protein – but it does not tell you how much of that protein is actually digestible.


Allowance allows you to account for disease, stress, environment etc. AFFFCO allowance determines what level of nutrients we need to put into a diet for a dog or a cat.


Requirement – the level of nutrient that will prevent the sign of deficiency – is the absolute minimum.


Gives a safety factor – to compensate for conditions that are not ideal – is more “practical” because it takes into account the variation.


Routinely considered in ration formulation now – to help deal with environmental build up of these chemicals N/P.


Does an animal feel hungry during infection? No – they have a lower food intake.


Energy expenditure on stress/disease/parasite conditions – increase nutrient requirement of the animal.


There are huge variations in some populations. Chickens – not lots of variation – basically all the same. Pigs – not much variation. Beef cows/Humans – quite variable.


What about the dairy cows that are out in pasture in -35 weather?? This wouldn’t be adequate for them.


Nothing is black in white – why? Because you are dealing with a population based on the average requirements.


Highly active sport animal, pregnant, lactating, geriatric, weight, age, etc.

3. Using Questions 1 and 2: Formulate and balance a ration using the feed ingredients available on a least cost basis with set limits (parameters)

Computer models Limits to production Animal health

Sequence of Events in Nutrient Deficiency

The discovery of most of the nutrients as essential dietary constituents has been accomplished largely with farm and laboratory animals.

Regardless of the nutrient deficiency the same sequence of events prevails:

Nutrient deficiency↓

Biochemical defect↓

Functional defect↓

Microscopic anatomical defect↓

Macroscopic anatomical defect↓

Morbidity (illness)↓

Mortality (death)

Nutrition Affects Health Status of Animals

Beef Cattle: Rumen Acidosis – amount and form of carbohydrates Rumen Impaction – high fiber, low energy and low protein roughage Low Fertility, Calving Difficulty – over-fat cows

Dairy Cattle: Ketosis – body condition, feed intake, liver metabolism (similar to pregnancy

toxemia in sheep) Fatty Liver Syndrome – body condition and feed intake Low Milk Fat Syndrome – amount and type of carbohydrate, low rumen pH Milk Fever – calcium, acid base balance Left Abomasal Displacement – body condition, exercise

Swine: Poor Milk Production – excess body condition Lameness – body condition, mineral and vitamin D nutrition Obesity in Sows – feed energy density, feeding system

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Happens in all animals. Linked to calcium, phosphorus and vitamin D.


Caused by diet – not enough structure in diet (fiber) and a combination of a lack of exercise.


Also associated with metabolic syndrome whos origin is also due to nutrition.


Effects beef cattle and dairy cattle – happens when you feed the animal too much energy – deposit fat in the liver – then they calf and lactate and become more susceptible to other illnesses.


Basically reflects body condition (linked to nutrition).


Basically where the whole rumen fermentation seizes up because not getting enough food and energy.


Happens when you feed too much grain – rumen fermentation produces too much acid.


Nutrition is probably the #1 cause of problems in livestock and pet animals (dogs and cats).


When dealing with herds, if 1 or 2 animals are ill – maybe they are indicator animals and there is something much larger going on in the herd. These animals may just be the ones most susceptible to the illness/nutrient deficiency. Other animals that do not get sick (yet) are called subclinical – the ones that get sick = clinical.


Tissue damage


Cell damage


Eg. Enzyme not functioning optimally leads to a functional defect.


We know a lot about what to feed livestock and laboratory animals – we do not know a lot about human nutrition because the model used is mice and rats.

Horses: Malnutrition - starvation Laminitis – carbohydrate overload Contracted tendons – minerals, rate of growth

Pets:Obesity, metabolic syndrome, etc.

Reasons for Continued Nutritional Study in livestock1. Genetic improvement of animals2. Increased artificial rearing3. Environmental concerns and Green House Gas emissions 4. Changing genetics of crops-feeds5. Reduced use of multiple protein sources; primarily reliance on a few feedstuffs6. Early weaning in swine7. New feedstuffs8. Changes in agronomic practices9. Narrow profit margins

Reasons for Chemical Analysis of Feeds and Feed Ingredients

For ration formulation: - Analyze feed samples for on-farm use- To develop feed data bases on feed composition- Regional and company data bases

To provide analyses for use in estimating available energy use of feedstuffs (TDN, Net Energy etc.)

To provide information to solve a production problem that may be feed related To place a market value on a feed To verify a commercial guarantee For use in a feed quality competition (forage quality)

[For Lab presentation:]Feed Sampling for Analysis:

Sampling technique is the most important cause of variation in nutrient values Method is important to avoid error

ForageHay: Penn State core sampler - 10-12 balesSilage: grab samples- 4 to 6 250 ml samples composited and mixed

Feed in bagsCore samples from 5 bagsBulk feed in a bin10 samples from different areas

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Alfalfa Hay/Grasses – Who has the best quality – helps to teach people how to grow good crops.


Once you know the chemical composition of the feed – you can establish a price of the feed.


Farmer gets pissed and goes to feed company and asks for compensation – feed company says no – then they go to court. You might get called as a witness because you took the samples Eg. High vitamin D = estrogenic effects = abortions.


Take feed samples, submit for protein/AA analysis – then you can see if there is enough or if quality is adequate. Usually it is not adequate.


Sometimes an animal nutritionist/veterinarian will say there is something going on with this pig operation – I am suspicious that these pigs aren’t getting enough protein or protein quality is not what they should be. Pigs growing more fat and not enough muscle.


Data tables on chemical composition of fees used in previous years.


Standard Practice on farms.


Use chemical analysis on the feed for livestock.


Typically you do not need to do chemical analysis on dog or cat food. Only do it unless you think there is something fucked up in there. Labour-intensive and costs money.


Increases the productivity, less drought


In Western Canada – we switched over to no tillage farming – we do not disturb the soil. Seed right into the soil from last year. Soil blows away, disrupt microbes. Loss of topsoil, lots of organic matter on the top of soil ( more fungal diseases ( Ergot, mycotoxins.


7 day - 3 weeks compared to 7-8 weeks in the past.


Same thing with human nutrition – not good to just eat burgers all day.


Becoming more and more dependent on a few dietary ingredients to feed animals. This increases the risk that a disease/deficiency will occur In USA: they feed swine/dairy cattle corn or soybean meal. In Canada – we have peas, lentils, mustard, canola, corn, soybean meal. Lots more options.


Plant breeders want better productivity, more yield /acre, disease resistance, etc. We have to constantly reassess these crops as an animal feed.


Along w/ antibiotic resistance – how do we minimize the use.


The animal we are dealing with today is very different from the animals we had 10-20 years ago – this changes their nutrient requirement. 40 years ago dairy barns made 4000kg of milk/year. Today, dairy barns can make 12000 kg of milk/year.


40-50% of pets are now considered overweight.


Mineral and calcium deficiency are common problem in horses.


Owners least educated and do not feed the horse.

- Mix on a flat surface on paper- Store in a tightly closed container- Refrigerate if necessary

Nutrient Groups

We know which the nutrients are, but how do we measure these chemically?

Chemical analysis using the Proximate Principles ‘Weende System’

Water

Crude Protein (CP; assumes 16% nitrogen in real protein) 100 ÷ 16 = 6.25

therefore N % x 6.25 = CP % Crude Non Protein N (NPN) + true protein[Melamine is a NPN]

Ether extract (fat)

Ash

Crude fibre (older method)

Nitrogen Free Extract (non-fibre carbohydrate or starch)

In flow diagram next page:

Ash is further analyzed for minerals by atomic absorption spectrophotometry.

Fiber is measured as Acid Detergent Fiber (ADF) and Neutral Detergent Fiber (NDF).

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Crude fiber not used any more (especially in ruminant feeds).


This is calculated by different – know how much protein, fat, moisture, ash, crude fiber – weight of feed – the difference has to be starch.


Put food in oven – analyze the ash that is leftover.


Now there is a lot of doubt in the pet food that china makes.


Was found in pet food, baby formula manufactured in china, etc. They were adding melamine to increase the nitrogen and to artificially elevate the crude protein and increases their profit.


We assume true protein contains 16%.


We measure the nitrogen – convert it to protein. Crude protein – means it’s a measurement of protein based off the nitrogen levels. If you take a soybean meal/wheat – it is not going to all be real protein – there are also some non-protein nitrogen compounds as well (nitrates, etc). Nitrogen contaminated w/ NPN.


We analyze these on a standard measure.

Flow diagram Proximate Analysis

Crude fiber vs ADF and NDF (see next)

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FIBRE IN FEEDS (REALLY UNDERSTAND THIS).

Crude Fibre(CF) = indigestible by monogastric animals, but not in ruminants

Van Soest Fibre or Plant Cell Wall method (for forages)

VAN SOEST DETERGENT SYSTEM

Ground Forage Material Digest w/ neutral detergent ND solubles(cell content) + ND insoluble fiber (cell wall components).

ND insoluble fiber digest with acid detergent AD solubles (hemicellulose – cell wall with N) + Acid insoluble fiber (cellulose w/ lignin).

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A slide about this will be put onto PAWS.


ADF = acid detergent fiber = LIGNIN + CELLULOSE NDF = neutral detergent fiber = HEMICELLULOSE + LIGNIN + CELLULOSE. NDF – ADF = hemicellulose If you provide too much NDF (lots of fiber) ( slow down metabolism and fermentation – takes longer to digest (passage time increased) ( less ability to absorb nutrients (May put animal into ketosis (b/c animal not getting enough energy). Animal will start to utilize body fat for energy – liver can’t deal with it ( ketosis.


Cell wall of the plant contains all of the fiber – containing cellulose, hemicellulose and lignin. Primary cell wall is exterior and is a mixture of lignin and cellulose (intertwined). Secondary cell wall is interior and is mostly hemicellulose. Acid Detergent Fibers – lignin and cellulose Neutral Detergent Fibers – is hemicellulose + ADF. Most of the fiber is assoc. with the primary cell wall.


When you look at plant cell theres the interior that contains the cell contents.


Designed to measure the different components in the plant cell wall present in the grass/silage/forage crop.


Older method – no longer used in ruminant animals.

Acid insoluble fiber digest w/ 72% sulfuric acid (H2SO4 – breaks down cellulose) Solubles (cellulose) + Acid insoluble lignin.

Used primarily for forages

Extraction with neutral or acid detergent solutions

Partitions the fiber component into soluble and insoluble carbohydrate

Fiber fractions are called neutral detergent and acid detergent fiber (i.e. NDF and ADF)

a. Neutral Detergent Fibre (NDF) includes

Cellulose (beta glucose linkage)

Lignin (phenolics)

Hemicellulose (xylose, arabinose, ribose

b. Acid Detergent Fibre (ADF) includes

Cellulose

Lignin

c. Acid Detergent Lignin (ADL)

Example Dairy Feeding:

ADF 19-21% of DM

NDF 30-32% of DM (early lactation 28%)

NDF digestible, slowly degradable

More gradual organic acid production

Increased saliva flow higher HCO3- secretion buffering

Reduced risk of rumen acidosis

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With NDF its more gradual organic acid production. We now have NDF as a functional food – it is fiber. Stimulating receptors in the mouth/rumen to increase saliva production (w/ lots of bicarbonate) – induces increased buffering capacity of the rumen. High NDF = more saliva flow = more structure in the feed ( animal chews more ( more saliva production ( less susceptible to acidosis.


Starch almost flash ferments into organic acids (acetic acid, butyric acid, propionic acid) – drives down blood pH & drives down alkaline reserve – can cause animal to go into metabolic acidosis. In rumen it causes pain receptors to be activated – it reduces rumen motility – gas build up in rumen = BLOAT (can be lethal).


Acid load is not instant – it increases over time.


IF YOU GO BELOW THESE RECOMMENDED VALUES – you put animal at risk for acidosis and displaces abomasum.


Targets we must keep in mind when formulating feeds for animals.


Dry Matter.


Includes everything!

Other Typical Feed Analyses

silage pH (3.8 – 5.0) and C4 butyric acid

bomb calorimetry for gross energy (GE)

amino acid analysis

NIR: near infrared, estimates protein, energy and fibre using equations

feed microscopy, identify ingredients and contaminants

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If you find butyric acid, it indicates that the silage is not very good.


Silage = grass, barley, grain ( cut at a certain maturity – allowed to dry in the field – then put into a pit and allowed to ferment.


On a feedlot animals are being fed diets that are 85% grain ( these animals are always on the edge of acidosis.

WATER CONTENT OF FEEDS (IMPORTANT/CONFUSING SECTION – WILL BE A QUESTION ON THE FINAL EXAM – NEED TO KNOW HOW TO DO THESE CONVERSIONS).

1. Reported as “As Is” OR “As Fed” OR “Air-Dry”

2. Standardized to 90% DM, is also termed Hay Equivalent (HE) as most hay has around 90% DM

3. Standardized to Dry Matter (DM) Basis (0% moisture or 100% DM)

2 and 3 are done to standardize comparisons of feed ingredients and price

Remember: More water or moisture in a feed dilutes the nutrient content or density.

Less water concentrates the nutrient content or density.

EXAMPLE : Dog food

As fed = 35% DM (65% water) and 3% CP

Convert CP% to a dry 100% DM basis

= 3% CP X (100 % DM / 35 % DM) = 8.57% or

3% CP / (35 % DM / 100 % DM) = 8.57%

Hay and Hay Equivalent: 10% CP on a 87% DM basis = 10 x 90/87 = 10.34% CP as HE (90% DM)

(drier feed thus increasing nutrient density)

LAB - FEED CLASSIFICATION

CONCENTRATES

High in energy, low in fibre contenthigh energy - (and can be high protein)

Cereal grains: barley, corn, oats, wheat

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WILL BE COVERED IN THE LABORATORY!! IS STILL IMPORANT NOT COVERED IN CLASS.


Basically going to less moisture so you get a higher protein content.


Take 3% crude protein – multiply by 100/35 = 8.5% protein. QUICK WAY: 3% divided by 0.35 gives the same thing.


70% moisture compared to 30% nutrient 70% will have more dilute nutrients. When you get lab problems – are you taking water out or putting water in (diluting).


This is the one WE will focus on primarily – it is the most common.


10% moisture base or 90% DM. Most hay has 90% DM Used in cattle, swine and poultry feeding.


This means that is the level of nutrient in the food as it sits right in front of you (as you give it to the cow/calf).


No water = 100 % Dry Matter

Grain milling by-products: wheat bran, rice bran

Food processing by-products; molasses, distillers and brewers byproducts

Roots and tubers; turnips, potatoes, cassava

PROTEIN SUPPLEMENTS

Contain more than 20% protein

Oilseed meals; canola meal, soybean meal, cottonseed meal, linseed meal

Grain legumes; peas, lentils, beans, lupins

Animal proteins; fishmeal, meat and bone meal, feather meal nitrogen/protein for ruminants

Non protein nitrogen; urea, ammonium phosphate

Rumen bypass protein; dehydrated alfalfa, corn gluten meal

Roughages

Bulky material with high fibre content and low nutrient density. Protein and mineral content varies widely

Pasture

Silage (see next page)

Hay

Straw

Roughages can be legume or non-legume

Legume is a N fixator and has higher protein content – clover, alfalfa (lucerne)

Non-legume – grass silage, barley silage, corn silage, grass hays (bluegrass, timothy).

FEED ADDITIVES

Mineral supplements, limestone, salt

Vitamin supplements

Amino acids

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Drugs; antibiotics, ionophores

Preservatives; antioxidants, mold inhibitors

Buffers; sodium bicarbonate

Flavors; anise, fenugreek, licorice

Pellet binders; lignosulfonate, bentonite

Silage process: (slide)

High quality silage low butyrate, high lactate and low pH

PHASES: I: Oxygen 12-24h II: Acetic acid 24-72hIII: low pH low acetic high lactate 3-4dIV: Preserved with lactateV: feed out with oxygen infiltration spoilage and mold formation

GENERAL RATION CHARACTERISTICS

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SWINE: Cereal grains 70-80% OiI meals (soy or canola meal) Mineral-vitamin supplements Synthetic amino acids

DAIRY COWS: Forages (hay-silage) 40-95% Cereal grains Oil meals and byproduct feeds Proteins not degraded in the rumen ie. blood meal, various heated proteins Mineral-vitamin supplements Buffers (sodium-bicarbonate)

Lecture: Digestibility:

The proportion of the feed not excreted in the feces, and which is therefore assumed to be absorbed (it is implied that nutrients which disappeared from the gut were absorbed in a useful form, but this is not measured!)

Methods of Determining Digestibility

Measurement

Total collection

Indicator methods

Estimation

Chemical analysis ie. ADF, or more complete analysis

Enzyme laboratory methods

Artificial rumen (in vitro)

Rumen nylon bag (in sacco)

Mobile nylon bag; moves through part or all of the intestine in surgically altered animals (pigs)

Total Collection Method

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Porous bags – enzymes and stuff can flush through the bag.


Simulation feedstuffs in vitro.


Chromium – to see how much of the mass is being diluted/concentrated though the GI tract.


Collect feed ( then feces afterwards then chemically analyze the feed/feces.


Not actually measured – can’t do it – unless u put a catheter in the portal vein of the liver – to see nutrient flow from the GI tract. Practically impossible.


Hindgut fermentation is also fermenting feed – some feed may have not been used by the host – but are then used by hindgut microbes. Host benefits by absorbing VFAs – no AA transporters in the colon/hindgut . No glucose transporters in the hindgut Only partial benefit to the host – not everything that is fermented is used by the host.

Animals are fed a single feed or a diet of known composition for a number of days and during the latter part of the period all feces are collected;

After 10-14 days for monogastrics, 20-30 d for ruminants.

Must know amount and composition of feed consumed and amount and composition of feces voided.

Then calculate:

Apparent Digestibility, %

Nutrient intake - Nutrient in feces x 100 Nutrient intake

True Digestibility, %

Correct for endogenous excretion

Nutrient intake - (Nutrient in feces - endogenous nutrient) x 100 Nutrient intake

True digestibility is used mainly for protein and fat. Can also be used for minerals.

Index or indicator method

An indicator substance is mixed with the diet or given by bolus:

Bolus characteristics:

Not absorbed (No effect on the animal)

Not altered in the gut

Excreted uniformly in the feces

Readily measured

Example: Chromium Sesquioxide (Cr203) green color

FACTORS AFFECTING DIGESTIBILITY

Animal Factors

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Not all of the components of the feces are from the feed stuffs – there are also endogenous excretions - mucousal cells, enzyme residues, etc.


Nutrient intake (kg) – nutrient in feces (kg) / nutrient intake (kg) Is not completely scientifically correct.


The fermentation microbes must adapt to the new diet before you can analyze the collections.

Type of Digestive Tract

Low digestibility of plant cell walls (fiber) by monogastrics

Age of animal

Level of feed intake

Health status

Feed Factors

Feed composition (type of plant, stage of maturity, amount and type of fibre)

Processing of feed, fine particle size, part of plant

Additives, enzymes

Associative or Matrix effects (one feed changing the digestibility of others)

Effect of Environment

Temperature: low temperature increased feed intake faster rate of passage lower digestibility (ruminants)

Other methods used to evaluate feeds and determine nutrient requirements: Used in combination, may overlap

1. Dose-Response Trialso Growth (dietary amino acid level) o Biochemical or functional defect (Thiamin or Vitamin A) o Nutrient balance (protein, trace minerals)

2. Factorial Method (energy, protein)o Maintenanceo Growtho Production (milk, wool, activity)

3. Digestion Trialso Measures availability of nutrients in feedso Whole digestive tract or part of the tract in surgically altered animals, rumen

fistula, or duodenal canula

4. Clinical-metabolic evaluationo Biochemical, function, microscopic-macroscopic defects

5. Use of statistical analysis

EXAMPLE OF DIGESTIBILITY BY TOTAL COLLECTION19


We want to know what goes into the small intestine and what comes out of the ilium – to see what was absorbed. Can also go into large intestine – to see how the feed influences the microbiota.


For 1 kg protein/milk should come from 0.8 kg of feed per day – to calculate how much the animal should have consumed to produce that much protein/milk.


Plot a graph of growth (y-axis) and % amino acid (x-axis). Keep adding amino acids until the growth plateaus – where it starts to plateau is the dietary requirement


Can provide the animal with some extra grain – which has a better digestibility than their regular feed ( compensates for low digestibility in low temperatures.


One feed can influence the ability of the other feed. Interact with each other.


Can be added to feed to get better protein digestion, etc.


Grinding reduces particle size – increases the surface area of the feed – more area for digestive enzymes to attack the feed. Remember when you grind feed – you gotta think of the functional aspect of the feed.


Cytokines (IL-1) interfere w/ apetitie Allergic reactions – when you feed soymeal to baby pigs you get allergic reaction and inflammation of the gut (not useful for absorption).


Health status effects efficiency of metabolism itself. Parasites (tapeworms, coccidiosis) – causes damage to the gut wall. This displaces absorptive epithelium with scar tissues (permanent) – causes loss in absorptive capacity – can never absorb as efficiently as they did before the infection.


High input of feed – less residence time in the digestive tract itself (less time for enzymes to act on the feed stuff to depolymerize proteins, starch, etc. And less time to absorb the nutrients = lower digestibility.


Older animals have low digestibility; young animals have high digestibility.


Ruminants – well adapted to consuming/digesting – relatively undigestible feeds (high in fiber/cellulose). Pigs have low ability to digest high fiber/cellulose diets.

• Steer 300 kg live weight. • 14 day adjustment period on experimental ration • 5 day feed intake, DM; 6 kg/day x 5 days = 30 kg • 5 day fecal collection: Total wet feces = 40 kg

DM % in feces = 30% Total dry feces = 30% of 40 kg = 12 kg • Dry matter digestibility = 30kg DM intake - 12 kg DM in feces x 100 = 60% DM Dig. 30kg

• Crude protein digestibility =15% CP in feed DM 17% CP in fecal DM

CP digestibility =

(30 kg x 15%) - (12 kg x 17%) X 100 = 55.6% CP 30 kg X 15%

• Digestibility of other nutrients

Gross energy; DE, kcal/kg Ether extract ADF, NDF Starch or nitrogen free extract

ENERGY

Required by all animals for:

Maintenance, growth, physiological functions of living tissue

Thermoregulation

Locomotion

Energy Measurement: Calorie

“Quantitatively, energy is the most important element of diet.”

Source: CHO, Lipids (fats) (protein)

- Animal will eat to satisfy its energy requirement !!!!!!!

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The energy content of the feed will determine how much of the feed will be eaten. High energy content feed – animal will eat less and visa versa.


Source is protein, carbohydrates and fat.


Protein that was eaten – protein that was shit out.


Fairly normal for a forage type diet.


THIS IS APPARENT DIGESTIBILITY. Must correct for endogenous excretion to get TRUE DIGESTIBILITY.


Take what you ate then subtract what you shit out.

- Determines the daily intake of feed (the energy level of the food will determine how much food the animal will eat) subject to physical capacity

- Thus energy level determines the overall intake of all nutrients

- Other nutrients like protein must be balanced to the energy intake. For pets often concentrations are expressed per 100 Kcal ME, such as g protein per 100 Kcal ME

- Therefore a diet with high energy content must also have higher levels of other nutrients to ensure the animal will receive the daily requirement (such as grams per day) for all nutrients (because the animal will eat less)

- A diet with lower energy content will cause the animal to eat more feed, and therefore other nutrients can be at a lower level also. But physical capacity of the GI tract will limit how much feed the animal can eat (upper limit). Chemostatic control vs physical control.

BIOENERGETICS- Energy sources, utilization and metabolism

All animal functions and biochemical processes require a source of energy

ENERGY TERMINOLOGYCalorie (CAL) = energy to raise 1 g water from 14.5 to 15.5 C

Kcal = 1000 calories

Mcal = 1000 kcal (also called a therm) = 1000000 calories

Joule (J) = 4.184 cal

BTU = 252 cal (not used in animal nutrition)

Calorie system: North American feed industry, US research

Joule system: UK Feed industry and research and Canadian research publications.

GROSS ENERGYHeat released from complete oxidation of a feed can be measured in an oxygen bomb calorimeter

Nutrient Kcal /g Carbohydrate mean 4.20

Protein mean 5.6521


Max amount of energy that you can get out of 1 g of feed.


Complete combustion of a feed into CO2 ( put into an oxygen bomb calorimeter ( basically trying to see how much heat is produced by the explosion.


British thermal unit.


Physical control: the physical capacity of the gut – how much food can be held in the digestive tract.


Energy intake is a function of the energy requirement of the animal (chemostatic control) Animal will be hungry – low blood glucose – low insulin. Animal is satiated when there is high blood glucose and high insulin levels


Gram of protein/100 kilocals of metabolizable energy??


Gotta figure out energy level before you even consider protein content – because the energy content will determine how much the animal actually needs – then you can figure out how much protein to put into it to meet the animals daily requirement with the amount they are eating.

Fat mean 9.30

Ash (minerals) 0

Water 0

Glucose 3.78

Glycine 2.04

Lysine 4.84

Ethyl alcohol 7.11

Methane 13.3

Acetic acid 3.49Propionic acid 4.96Butyric acid 5.95

Gross energy is influenced mainly by water, fat and ash content of a feed and to a lesser extent by the type of carbohydrate, fat and protein

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IMPORTANT VOLATILE FATTY ACIDS. Acetic Acid (C2) Proprionic Acid (C3) Butyric Acid (C4) Ruminants are not very good at utilizing glucose ( thus they rely on the fatty acids for energy. But they need glucose for synthesizing lactose for milk production They use propionic acid – which can be converted to glucose??


Almost as high as fat – this is why alcohol is bad for you.

Gross Energy of Feed (GE) (Heat of Combustion)

Fecal Energy (FE) (30%)1. Undigested feed2. Enteric microbes & their products3. Excretions into the GI tract4. Cellular debris from the GI tract

Digestible Energy (DE) (70%)

Urinary Energy (UE) (5%)Gaseous Products of Digestion (methane) (5%)

Metabolizable Energy (ME) (60%)

Heat Increment (heat of nutrient metabolism) Heat of Fermentation (from the rumen, cecum, large intestine)

Net Energy (NE) (40%)

Maintenance Energy Productive or Recovered Energy 1. Basal Metabolism 1. Tissue Energy (muscle, fat)2. Voluntary Activity 2. Lactation (milk)3. Thermal Regulation 3. Conceptus4. Product Formation 4. Wool, Hair5. Waste Formation and 5. Work

Excretion

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Net Energy is 40% of the gross energy intake.


Microbes generate heat themselves.


We can determine the inefficiencys in the metabolism in ruminant animals. Synthesizing protein, lactose or body fat – all have inefficiencies assoc. with them. Think of a car – energy in gasoline is metabolizable energy How much energy in gasoline is actually being converted into horse power to move the car?? 30% ( so 70% is lost through heat – this is why cars have radiators.


Typically, what you experience after a meal high in protein.


The measure used for cats/dogs/humans/poultry/swine NOT ruminants It is digestible energy – with correction for energy loss in the urine ~10%.


An issue with ruminant animals ( not to monogastric animals


Protein breakdown is the most important source of energy in the urine These compounds generate urea, etc (nitrogenous waste compounds).


Metabolic pathways are occurring – there are some inefficiency’s – some of these end up in the urine. Digestible Energy is: Gross Energy – Fecal Energy


THIS FLOW DIAGRAM WILL BE ON EXAM


Gross energy goes into: Fecal energy (30%) Digestible Energy (70%)

Digestible Energy (DE)

DE = Gross Energy – Fecal Energy

DE/GE = 80% for pigs and poultry (& dogs/cats)

DE/GE = 70-80% for ruminants fed concentrates (on grain based diets)

DE/GE = 50-60 % for ruminants fed roughages (hay)

Metabolizable Energy (ME)

Takes into account additional losses arising from the absorption and metabolism of the feed, such as energy loss in urine and energy lost in gaseous products of digestion.

ME = DE – (UE + GPD)

ME is usually in the range of 82 % of DE in ruminants and 92 % in pigs

GPD - Gaseous Products of Digestion:

Results from fermentation in the digestive tract. The gases produced contain energy and thus result in energy loss.

Methane, Hydrogen and Hydrogen Sulfide

Non-ruminants: <1 %

Ruminants 5 – 15 % (significant)

Efficiency of ME use:

ME use for maintenance, 65 % in ruminants

ME use for lactation, 65 % in ruminants

ME use for growth and fattening, 45 % in ruminants, 70 % in non-ruminants

Net Energy

Net energy refers to the part of the feed that is completely useful to the animal to maintain itself or to produce growth, milk, eggs, etc.

NE = ME – Heat Increment

HI - Heat Increment

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When an animal consumes a meal – and you measure heat production (cal/min or cal/hr). After meal there is an increase in heat production (called a metabolic flush). Most of the Heat production comes from nutrient metabolism (pathway metabolism – kidney, liver, muscle – are activated & have inefficiencies that lead to heat production).


He wont ask us these numbers – but you need to know the rough losses as you go from DE to ME to GPD.


Feeding ruminants roughages is better for nutrition, but it is bad for the environment (green house gas production).


Larger in the ruminant because they produce methane (a form of energy). The methane losses from rumen fermentation represents about 10% of the energy loss from the animal.


Digestible energy for ruminants depends on the amount of fiber they are getting in their diet.

Increase in Heat Production Following Eating When the Animal is in a Thermo-Neutral Environment.

Work of Digestion = 5 %

Heat of Fermentation = 15 %

Nutrient Metabolism = 80 %

Factors Affecting Heat Increment

Digestibility of ration high then lower HI

Makeup of Ration Forages have higher HI than concentrates (more heat of fermentation and C2)

Level of Feeding

How the Feed is Utilized(In ruminants the C2:C3 ratio, with C3 more efficient metabolism)

Amino Acid Balance (40%)

Nutrient Deficiency

Frequency of FeedingHigher frequency, lower HI

Injury or infection (30-40%)

NE - MAINTENANCE NE - PRODUCTION

BASAL METABOLISM GROWTH

HEAT TO KEEP BODY WARM FAT DEPOSITION

VOLUNTARY ACTIVITY ASSOCIATED WITH MAINTENANCE

REPRODUCTIVE PRODUCTS

MILK

WORK

Maximum Level of Energy Intake

For growth in most species = twice maintenance

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The amount of the energy intake is 2x that of what you need for maintenance. Maintenance requirement – maintains the animal and doesn’t contribute to growth.


Already discussed apparently.


Not chronic – if an animal has a fever, inflammation – then the energy to produce the fever is coming from somewhere and causes heat increment.


There are 10 essential amino acids (must be supplemented in the diet). Balance – the level of indiv A.A meets the requirement of the animal for that particular animal. There is no excess/shortage. When you feed a poor diet there can be excess/shortage in the diet: problems usually arise from methionine and lysine. Minor imbalances can cause major changes in the efficiency in protein metabolism – these inefficiencys show up as HEAT. High protein quality – low heat increment. Low protein quality – high heat increment.


More proprionic acid production in the ruminant – more efficient digestion. If you have butyric acid/acetic acid digestibility is less. Grain type diets swtich the ruminant to produce more proprionic acid (leading to more efficient metabolism) & LESS green house gas production


Increased digestibility – less digestion needed (less metabolic pathway activation) = less heat production.

For work in most species = twice maintenance

For lactation = two to four times maintenance

(dairy cows can take in 4x maint.)

Estimate of Feed intake kg DM/d:

Look up in NRC tables

Rough guide – express as % of Body Weight (BW)

Maintenance ~1.8 - 2.0 % BW

Peak lactation ~ 3.5-3.8% BW

Growth ~ 2.8-3.0 % BW

Determination of Net Energy Requirements and Feed Values

Feed values can be determined by measuring or estimating the various components of energy partition. The difference between gross energy and the components gives an estimate of NE.

Requirements can be estimated from energy stored in products (gain or milk) when a known amount of feed is consumed.

Stored energy (gain) can be obtained from slaughter trials and carcass analysis or various estimates of carcass composition:

Specific gravity

Ultrasound

Isotope dilution techniques

Combinations of methods can be used for both feed values and requirements.

Other Energy Measuring Systems:Physiological Fuel Values (PFV) (or Atwater or 4-9-4 or ME)

A form of ME where gas loss is ignored (used in dogs, pigs and people)

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More practical way of measuring metabolizable energy in the feed stuff. This is used a lot in human and pet nutrition. Might use this approach in practice.


Measure the Sg of the body in water – can give u an index of how much bone/fat/muscle is present.


If you have an animal that weighs 500 kg – you can expect the animal to eat 10 kg of DM per day at the 2% level.


Know well: we’ve heard this term over and over again.


Lactation represents an enormous energy drain – for lactating dogs maintenance might be as high as 7.

Nutrient GE (kcal/g) Urine Dig Factor Protein 5.65 1.25 92 4.0

NFE (CHO) 4.15 --- 98 4.0

Fat 9.4 --- 95 9.0

Measured as kcal/gExample:

Bread, 100g of DM: 12.2 g CP, 2.3 g fat, 66 g of NFE

(12.2 x 4) + (2.3 x 9) + (66 x 4) = 334 kcal ME

For pet foods:

• Modified Atwater factors for processed diets

▫ Carbohydrate: 3.5 kcal/g

▫ Protein: 3.5 kcal/g

▫ Fat: 8.5 kcal/g

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Using 4-9-4 rule over estimated the ME in pet food so they adjusted the Atwater values for pet food. Can still use 4-9-4 for human diets (standard).


Gotta know this! It’s a standardization based on averages! There is variation. Have to keep in mind that the food you may be dealing with might be different. This approach is not used for farm animals.


Nitrogen free extract.


On average 1.25 kcal of the energy produced from protein ends up in the urine – due to urea ending up in the urine. Protein on avg has a 92% digestibility. If you take 5.65-1.25=x then apply the 92% digestibility then you end up with 4.0 kcal/g of ME (metabolizable energy).


Have the 3 nutrients that generate energy – and the gross energy that each produces (GE).

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Use circled thing at the bottom to covert TDN to Mcal of DE.


TDN is primarily used in ruminant diets – mostly beef cattle and sheep. Odd to measure in kg and not calories.

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TDN is somewhere b/w DE and ME. Digestible Energy – after you deduct fecal energy loss. PFV = physiological fuel values. TDN corrects for fecal and urinary energy losses.

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Proximate Principles: water content, crude protein, crude fiber, etc. 50.2 /.9 (corrects for a 10% water content) = 55.9% DM


Applies well to forages – if you know the acid detergent fiber content of the feed to get TDN.

Calculating Maintenance Energy Requirement

Basal Metabolic Rate (BMR) or Basal Energy Requirement (BER)

70 X BW kg 0.75 (ME kcal/day)

Fasting (in monogastric animals)

At rest

Thermoneutral

Brain, liver, heart and kidneys make up about 5 % of body weight, but account for 60 % of basal oxygen consumption.

Muscle makes up about 40 % of body weight, and accounts for 25 % of basal O2 consumption in monogastrics.

In ruminants, Resting (fed and not fasting) Metabolic Rate is used (RMR):

77 X BW kg 0.75 (ME kcal/day)

Voluntary activity

Body temperature regulation

Waste formation and excretion

Maintenance Estimate

Is BMR X 1.2 to 1.8 depending on activity

__________________________________________

Canine (dog) daily energy requirements (ACVN)Unit: In Kcal ME/kg BW

Resting Energy Requirement (RER) = 70 x Wkg0.75

OR 30(BW) + 70 (for dogs between 2 and 45 kg)

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Used for FARM animals: This is not for growth/lactaction – it just accounts for the maintenace of the animal. You have to estimate the animals activity to decide which number to use.


Higher because the animal still has some digestive function.


You cant really fast a ruminant animal – you’d have to starve it for like a week (inhumane).


AKA Basal energy requirement – is the lowest rate of metabolism required to maintain body function as is in a fasted animal (no digestive function), in a thermoneutral environment (no expense of energy to cool off/warm up). Basically the thing you are measuring is the actual amount of energy to maintain the body mass. Quite similar over a wide range of species. BMR is controlled by thyroid hormone.

Maintenance (0.8 to 1.6 x RER): Healthy, neutered adult 1.6 x RER

Intact adult 1.8 x RER

Obese prone 1.4 x RER

Weight loss 1.0 x RER

Geriatric 1.1 x RER

Work:

Light 2 x RER

Moderate 3 x RER

Maximum 4-8 x RER

Growth:

Under 4 months 3 x RER

4 months to adult 2 x RER

Lactation: 4 – 8 x RER or free choice feeding

Feline (cat) daily energy requirement

Same basis as for dogs

Resting Energy Requirement (RER)

= 70 x Wkg0.75 or 30(BW) + 70 (between 2 and 45 kg)

Average, neutered healthy adult 1.2 x RER

Intact adult 1.4 x RER

Active adult 1.6 x RER

Obese prone 0.8 x RER

Critical care 1.0 x RER

Geriatric 1.1 x RER

Lactation 2-6 x RER

Growing kittens 2.5 x RER

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Not very practical – would be hard for an animal to eat 8x RER in their feed. If they cant comsume this from their diet – they will take energy from their body stores (fat, carbs etc). Very early after parturition the voluntary intake of food is not enough for lactation – they will rely on mobilization of body fat.


Very physically active dogs: sled dogs, dogs working for police.

Caloric Restriction and Longevity

Caloric restriction of 10-30% below ad libitum extends life span and health span, including brain and behavioural function. First reported by McCay, 1935. J of Nutrition, 10: 63

This has been found with many species: dogs, rodents, fish, nematodes, spiders, flies, protozoa, primates including humans

Many theories:

Reduced growth rate

Reduced body adipose tissue

Lower metabolic rate

Reduced plasma glucose-insulin fluctuation??

Less oxidative cell damage from hydroxyl radicals, peroxides, etc. (mitochondrial membrane)

Protection from acute stressors or the general protective action hypothesis

2015

A Periodic Diet that Mimics Fasting Promotes Multi- System Regeneration, Enhanced Cognitive Performance, and

Healthspan

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Not actually understood – but there are theories about why 10-30% reduce in caloric intake increases an animals live span.

Highlightsd FMD rejuvenates the immune system and reduces cancer

incidence in C57BL/6 mice

d FMD promotes hippocampal neurogenesis and improves cognitive performance in mice

d FMD causes beneficial changes in risk factors of age-related diseases in humans

In BriefBrandhorst et al. develop a fasting mimicking diet (FMD) protocol, which retains the health benefits of prolonged fasting. In mice, FMD improved metabolism and cognitive function, decreased bone loss and cancer incidence, and extended longevity. In humans, three monthly cycles of a 5-day FMD reduced multiple risk factors of aging

CARBOHYDRATES IN NUTRITION

Carbohydrate is a translation of the French term “Hydrate de Carbone”

o They contain H and O in the proportion found in water

They are the primary product of photosynthesis in plants

There is no specific individual carbohydrate requirement for animals but some carbohydrate is needed for metabolic functions

Dietary carbohydrate type and amount are related to health

FUNCTIONS OF CARBOHYDRATES

Energy Source

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Include fiber.


Glucose is required for brain function. Glycerol synthesis is from glucose ( if you want synthesis of fat tissue – you have to synthesize the backbone from glucose. Glc absorption, and gluconeogenesis (glc from a.a).


Carnivores lack the enzymes for digestion and absorption for glucose

Structural component of other compounds

-non essential amino acids

-lipids (glycerol synthesis)

Anti - ketogenic (prevents breakdown of fat and generation of ketones)

Protein sparing effect

Bulk (fiber)

Palatability (or influence food preference) –Makes food Sweet

Structure, water holding capacity in processed foods and feeds

Pre-biotic

CLASSIFICATION Monosaccharides (5 and 6 carbon)

Disaccharides

Trisaccharides

Polysaccharides

Pentosans

Hexosans

Mixed Polysaccharides

CARBOHYDRATES Large amounts in plants

o Starch (65%-70% of cereal grain)

o Cellulose (up to 40% of forages)

o Hemicellulose

o Pectin

Small amounts in animals

o Glycogen

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Carnivores have been exposed to very little carbohydrates – have not developed a system to metabolize carbohydrates – when they do eat it they don’t get much energy out of it. Eg. Salmon, tigers, cats, etc.


Lots of carbohydrates in cereal grains as well as root plants (potatoes, cassava, etc).


Polysaccharides are “complex” molecules of carbohydrates and monosaccharides are the most basic type of carbohydrate.


Meaning that some carbs provide sugar compounds that are nutrients for the microflora in the gut – especially for the production of milk.


Makes sure A.A are being used to make proteins instead of gluconeogenesis.


Ketogenesis typically occurs in monogastric animals during a fasting event. Adipose tissue mobilization occurs because of low blood glc and low insulin. Basically prevent lipolytic breakdown of F.A which makes ketones

o Glucose

o Chitin (long-chain polymer of N-acetylglucosamine)

HOMOPOLYSACCHARIDE: CHO contains only ONE TYPE of saccharide unit

1. STARCH: slides basic unit: alpha-D-glucose

principal starch form in CEREALS (seed energy storage)

two (2) forms of starch exist: AMYLOSE and AMYLOPECTIN

AMYLOSE alpha 1,4 linkage only – straight chain 15 – 30 % of total starch in most plants

soluble in water

molecular wt: 10,000 – 100, 000 (glucose = 180)

exists in alpha-helical coil: retains IODINE – blue color

degraded by both and β – Amylase

high amylose grains - lower glycemic index

AMYLOPECTIN: alpha 1,4 linkage with alpha 1,6 linkage at branch points

70 – 85% of total starch

NOT soluble in water

Molecular wt: > 1,000,000

Limited coil – cannot retain iodine red purple color

Lots of side chains = 19 – 20 glucose unit

Degraded by - Amylase only

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Whereas amylose is degraded by both alpha and beta amylase.


Very large macromolecule.


Most common form of starch.


The appearance of glc going into circulation appears over a longer period of time.


Provides energy for germination of seeds & starts plant growth.


Very large macromolecules.


Present in the shell of shelled animals.

2. GLYCOGEN: animal starch

Basic unit: alpha – D – glucose Exists in small amount in LIVER and MUSCLE Similar to AMYLOPECTIN in structure

Except HIGHLY BRANCHED – with shorter side chains

Water soluble

NO helical coil red color with iodine

3. CELLULOSE: Basic unit: β D – glucose With beta 1,4 linkage in straight chain

Highly stable and crystalline: no animal enzyme can digest it

Microbial CELLULASE can degrade it

COTTON is one of the purest form

Most abundant CHO in nature

4. INULIN: Basic unit: FRUCTOSE

High molecular weight, soluble in water

Found in roots and stems

Used extensively in metabolic studies

HETEROPOLYSACCHARIDE: CHO contain more than one (2 – 6) types of sugars

1. HEMICELLULOSE NOT ½ of a CELLULOSE

It is plant glue - sticky

β - 1,4 linked XYLOSE (a pentose) branched

complex mixture of glucose, mannose, arabinose and galactose principal component of plant CELL WALL

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5 carbon sugars. Humans and monogastric animals do not have enzymes that can digest beta 1,4 linkages!


Microbial fermentation in ruminants allows them to digest cellulose.

mammalian enzymes CANNOT degrade this, however, microbial enzymes do

2. PECTIN mainly POLYMERS of alpha 1,4 linked glucose

but also contain D-galacturonic acid.

Thus, no animal enzyme can break it

However, readily available to ruminant microbes

Found primarily in the space between CELL WALLS

Soluble in water

Non-CARBOHYDRATE

LIGNIN: Polymers of PHENYL PROPANE derivatives

Encases the cellulose and hemicellulose

As plant matures it becomes “woody”: lignification

Reduces digestibility of cellulose and hemicellulose

NO animal or anaerobic microbial enzyme can break it

SOME fungi and aerobic microbes can digest i

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Important for ruminant/swine nutrition – not really for pet nutrition (not present intheir feed)


They produce oxygen radicals (ROS – reactive oxygen species) and H202 that work together to digest lignin.


Not good in feedstuffs – makes it harder for enzymes to access cellulose and hemicellulose. Animals cant digest lignin. Rumen digestion also cant really digest lignin.


Helps to form the cell wall of plants – acts as a “glue”. Provides the plant with structural support.


Not digestible.


In ruminants its digested into volatile fatty acids.

Major Components of Lignocellulosic Biomass (Department of Energy USA)

Example of composition of wood

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Typical fibril can be 10 nm in diameter and 100-500 nm long (called whiskers). Don’t have to know these particular #s

DIGESTIBILITY OF CARBOHYDRATES

STARCH All species 80-100%

Cell Walls

Are in the Neutral Detergent Fiber (NDF) fraction: hemicellulose, cellulose and lignin

Digestibility:

Ruminants 50-90%

Horse 35-50%

Poultry 25-35%

Pig 05-30%

Dog 10-30%

Human 25-40%

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90% digestibility when lignin is low. 50% digestibility when diet is high in lignin.

Nutritional Classification of Starch Non ruminant (monogastric) system

Based on release of glucose from an in vitro assay using a pepsin-carbohydrase enzyme cocktail

Rapidly available glucose (RAG) Rapidly available starch (RAS) 20 min test Slowly digestible starch (SDS) 120 min test Resistant starch (may have similar effects as fibre)

Physically inaccessible (whole grain)Resistant granulesRetrograde starch (Amylose), B type granules

Glycemic Index: Rise in blood glucose after a test food is consumed

High GI Low GI

White Bread 100 Skim Milk 46

Glucose 140 Oatmeal 87

Instant Rice 124 Pasta 40-70

French Fries 107 Apple 34-76

Sucrose 83

DIGESTION IN RUMINANTSReticulum Rumen Omasum Abomasum

Reticulum: Receives feed from esophagus Pass feed to rumen and omasum

Reticular groove reflex (suckling reflex) to shunt liquids directly to abomasum (calf)

Eructation and rumination

Rumen:

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Reposition of the reticulum to ensure that gases do not build up – released out of the esophagus.


Oatmeal – low GI, but its good because it generates beta glucan (soluble fiber) – forms a gel in the gut and delays absorption of carbohydrates. Is a physical effect. When mixed with other food it still has the effect because its physical.


In vivo measurement of starch quality.

Bulk of fermentation: bacteria, protozoa, fungi

Digestion via microbial enzymes

Some mineral absorption

Volatile fatty acid absorption (extensive)

VFA’s are major end products of fermentation and provide a major source of energy to ruminants

Omasum: Regulates flow to lower gut: filter

Water absorption

Some mineral absorption (Mg)

Abomasum: Analogous to gastric stomach in non-ruminants

True Stomach

Digestive secretions (host)

Digestion of Carbohydrates by Ruminants

A. Ruminant’s saliva is different from the non-ruminants.

Saliva in the COW, SHEEP, and GOAT does not contain AMYLASE Output of saliva in ruminants is very high. It contains a lot of buffers. Without it,

rumen pH would drop markedly.

B. In the rumen conditions are ideal for bacterial and protozoal growth:

Fairly constant pH (pH 6)

Anaerobic conditions

Constant temperature

Constant supply of nutrients

Continuous removal of products of microbial digestion

C. Microbial enzymes break glycosidic bonds of fiber and starch

Bacterial cellulase and hemicellulase are capable of breaking the alpha or beta 1,4 bonds between CHO of cellulose and hemicelluloses

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Conditions needed for a continuous rumen fermentation system.


> ph 5.5


The same feedstuff that induces high saliva flow also contributes to motility in the rumen.


Acidosis in the rumen is bad. Bicarbonate neutralizes the acidity in the rumen fermentation system. Feedstuff containing lots of structure (hay, straw, silage) is going to give mechanical stimulation that induces high saliva flow. If you feed them a lot of ground feed, there will be little saliva flow even though the ground up feed is the one that results in the production of organic acids.


No need for amylase – because carbohydrates are digested by microbial enzymes not the host enzymes.


In monogastrics their primary energy source is glucose, fat, and protein. In ruminants has much lower levels of glc & insulin in their blood – because they don’t rely on absorption and digestion of carbohydrates in the small intestine. The energy they get is from absorption across the rumen wall.

Bacterial amylases also break starch into maltose. Protozoa engulf starch and digest starch inside their bodies.

D. Glucose is present in the rumen only transiently

Glucose is promptly used by microbes and through their glycolytic pathway converted into pyruvate.

Pyruvate is further converted into end-products called volatile fatty acids. These include ACETIC (C2), PROPIONIC (C3), BUTYRIC (C4) and other longer chain FATTY ACIDS.

This process is called FERMENTATION.

The VFAs are released from the microbes (as end-products) and are then available for absorption and utilization by various tissues.

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RUMINANT DIGESTIVE PROCESSES:

1. Feed enters the foregut and it may either be fermented by microbes or bypass the foregut altogether

2. Hence, digesta entering the abomasum included undigested feed and microbial cell mass

3. The proportions of these two components are extremely variable. Highly soluble feeds are extensively digested by microbes. Less soluble feed constituents largely bypass microbial degradation

4. Heat treated feed or feed treated with formaldehyde or coated with oil, so that high quality feed can escape the microbes in the rumen and thus can be break down in the abomasum and SI.

5. Ruminants absorb very little glucose

RUMEN FERMENTATION VS CECUM FERMENTATION:

What is the difference??

Major absorption site is at SMALL INTESTINE

Rumen is located before, and cecum is located after the small intestine

FACTORS DETERMINING AMOUNTS & PROPORTIONS OF RUMEN VFA

1. Level of feed intake

2. Frequency of feeding

3. Proportions of starch and fibre

4. Size of forage particles small particle size (finely ground) increases C3

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1. High feed intake & proportions of starch and fiber. The more energy in the diet the more VFAs produced. 2. If I have a steady input of feed then you get a steady fermentation system. If not a steady-state then you get fluctuations in pH which can affect the acid-base balance of the animal. Asserts selection pressures on the population. 4. Take a hay – chop finely/grind it – increase particle size – more surface area for microbial digestion. If you chop a hay – you can change the proportions of VFAs produced. If you grind/chop hay you get more proprionic acid and less acetic acid. If you add ionophores (class of antibiotics) to the diet they shift the fermentation pattern towards more proprionic acid Why is this important? Metabolic efficiency of the use of VFAs. Proprionic acid is the most efficient – preferred over acetic acid. Then you get more better feed efficiency @ a lower cost. 5. If you use ionophores – there is a positive impact on the environment because there is less methane gas produced.


In ruminants, fermentation results in energy fermentation (VFA, and microbial protein) occurs prior to abomasum and small intestine. Host can absorb this. In the horse – there is microbial protein production but it’s all excreted in the feces. Only VFAs, water, and B vitamins will be absorbed across the hindgut fermentation wall -- they cannot extract protein. Need to feed it as a monogastric animal – but you can feed it hay because it can do hindgut fermentation. What does a rabbit do?? Reconsume the feces – to get the benefit of the microbial protein.


We know how to make some feed bypass – to get the max amount of protein and the right quality of protein to the animal.


Microbes grow constantly and at some point they move through the omasum and abomasum and the small intestine and become a source of nutrients for the host. Microbes are a source of protein. Ruminants get protein from: feed protein, and microbial protein.


Rumen fermentation is not 100% efficient – some component will bypass and move into the small intestine where it may be digested in a similar way as monogastric animal. Solubility – how quickly the feed is broken down in the rumen fermentations system. Less soluble – more time to ferment.

5. Presence of rumen modifiers in the diet (lonophores) increased C3 (proprionic acid)

Alteration of ROUGHAGE : CONCENTRATE RATIO:

o Increased roughage intake results in

high acetic acid level

high milk fat

high methane production

higher rumen pH (lower acidity; 6.1 – 6)

o Increased concentrate intake results in:

High propionic acid level

Lower milk fat – higher body fat

Lower rumen pH (higher acidity; 5.5 – 5.8)

Alteration of the PHYSICAL FORM of the diet:

oGrinding and pelleting generally increase reactions which produce more Propionic acid (more rapid fermentation) and lower pH

Classification of Carbohydrate Fractions in Feed for CattleCornell - Penn State System

Fraction CHO type Rate of rumen utilization, % /h

A Soluble sugars 150-350

B1 Starch, pectin, beta-glucans 10-50

B2 Fermentable cell wall (NDF) 2-10

C Unavailable cell wall 0

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Does not get fermented at all.


At best only 10% is fermented every hour. High forage diets – much slower fermentation. Not really a good source of energy because they are fermented slowly.


50%/hr: half of what is consumed is fermented in an hour.


Soluble sugar (molasses, whey powder): get quick fermentation – meaning they will ferment in about 40 minutes (150%/hr) and 15 minutes (350%/hr). He calls it a “flash fermentation”. Produces a huge amount of organic acid in a short amount of time.


Proprionic acid is metabolized more effienciently and reduces milk fat. Not just high proprionic acid but just in general results from high VFAs C3 goes into gluconeogenesis in the liver primarily. It is the primary source of blood glucose. It goes into lactose in the mammary glands and results in volume. In milk the primary osmotic factor is lactose – it pull water from blood compartment and becomes milk. High lactose = high milk volume. Gluconeogenesis is ALWAYs on 24/7 – in monogastrics it only occurs during the fasting state. High C3 = High blood gluocose – triggers an increase in insulin. Insulin is lipogenic & anti-lipolytic. It makes the cow start to lay down fat. Energy from mammary gland diverted to adipose tissue because of INSULIN. Results in lower milk fat/ and high blood glc. Glc does not go into fat – instead it is used for brain function. Dairy cows gotta make 1-1.5 kg of lactose per day!


More acetic acid C2 and less C3 (proprionic acid. Promotes acetic acid producing bacteria. High acetic acid in rumen goes into fat synthesis (palmitic acid). Denovo fatty acid synthesis C2 and C4 ( C16:0 (palmitic acid) or C16:1 Also happens in mammary gland and leads to a higher fat content in the milk. Imporatnt because dairy farmers are paid for the amount of milk fat produces not the volume of milk. Methane production – is an energy loss.


Impacts rumen health (need forages in feed), and efficiency of feed in terms of supporting high growth etc.

CLASSIFICATION OF THE LIPIDS

Simple lipidsFatty acids: C2 to C24, saturated and unsaturated

Monoglycerides: monoacylglycerol

Diglycerides: diacylglcerol

Triglycerides: triacylglycerol

Cholesterol: cholesterol esters

Bile acids: cholic acid, taurocholic acid, glycocholic acid, etc.

Vitamin A: vitamin A esters

Waxes: esters of alcohols other than glycerol

Prostaglandins: hormones, essential fatty acids

Compound lipids: derivatives of phospatidic acid

Phosphatidylcholine (lecithin)

Phosphatidylethanolamine

Phosphatidylserine

Phosphatidylinositol

Sphingolipids

Other LipidsGlycolipids, Liproproteins,

Androgens, Estrogens

Chylomicrons, HDLs, LDLs, VLDLs

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Phospholipids are present in cell membranes.


No cholesterol problems in farm animals and not really in dogs/cats either.


Predominant form of fat used in nutrition. Found in adipose tissue and oils.

CLASSIFICATION OF LIPIDS

Lipid = All Ether Extractable material

1. SIMPLE LIPIDS-Esters of FA and Alcohols (mainly Glycerol)

FATS OILS

(SOLID AT RT) (LIQUID AT RT)

ESTERS OF FA AND OTHER ALCOHOLS: WAXES

2. COMPOUND LIPIDS

- Esters of FA and Glycerol containing 2 FA residues and another chemical grouping (eg. Choline linked through phosphoric acid: Lecithin)

3. DERIVED LIPIDS

-Substances derived by hydrolysis. Such as:FATTY ACIDS

ALCOHOLS (EG. GLYCEROL)STEROLS AND CHOLESTEROL

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Unsaturated FA are what make up oils.


More saturated, some unsaturated (Trans) fatty acids can also be found in solid fats. Most solid fats are of animal origin.

THE ROLE OF LIPIDS IN NUTRITION

Source of dietary energy (2.25 x carbohydrate)

Low heat increment - Minimize heat stress

Source of essential fatty acidso Linoleic (C18:2) and Linolenic (C18:3) Source of omega-3 fatty acids

Carrier of fat soluble vitaminso A, D, E, K

Cell structure and metabolic role

Feed/Food flavor (palatability)

Dust control, food/feed consistency,o Physical characteristics

Minimizes wear on feed handling equipment

LIPID CONTENT OF COMMON FEEDSTUFFS

Feed Lipid Linoleic % of DM % of Lipid

Alfalfa hay 2.7 16Barley silage 3.0 ----Brome grass hay 2.2 ----

Barley grain 1.9 42Corn grain 3.8 56Oat grain 4.5 33Wheat grain 1.6 40Wheat bran 6.0 55

Canola seed 40 65

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Canola seed has 40% oil – but we do not feed farm animals the whole seed we only feed them the canola meal (whats left after the canola oil has been extracted).


C18:2 – is high in grains (40-50%), forages/hay (16%). In animal sourced feed ingredients (meat meal, fish meal) there is not a lot of linoleic acid because animals cannot make it.


Plant material has about 2-3% fat, even in the cereals/grains it ranges from 1-6%.


Dust control, lubrication, consistencies. When lubricated you get better digestion, minimizes wear on the feed handling equiptment, etc.


Fat tastes good to animals.


If you feed these vitamins and do not have enough fat you get poor absorption efficiencies.


Some F.A. cannot be synthesized by the animal (they don’t have the metabolic capability) even though they are required. We are totally dependent on our diet to get these FAs


Fatty diets generate less heat, whereas protein (especially poor quality) generates a lot of heat.

Canola meal 3.5 ------Soybeans 18 45Soybean meal 1.0 40

Meat meal 9.0 2Fish meal 9.0 2Milk, whole 30 3Lard 98 11

FUNCTIONS OF BODY FAT

1. Energy Reserve: can be used during energy intensive processes (ie.

Lactation).

2. Insulation

3. Protection and Cushioning

4. Cell Membranes

5. Steroid Hormones

6. Bile Acids

Essential Fatty Acids (EFA)

Animals and people cannot synthesize EFAs, so these must be provided in the diet

EFAs are precursors for C20 compounds (eicosanoids) prostaglandins, thromboxane’s and leukotrienes intracellular messengers only (not transported in blood)

Most common mono-unsaturated FA in animals are: oleic (18:1c∆9) and palmitoleic (16:1c∆9).

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Can be synthesized de novo in the animal.


Essential for bodily functions – etc.

o (∆ delta, counted from COOH)

In animals and humans microsomes contain four Fatty Acid Desaturase enzymes, which can introduce desaturation at (Carbon) C4, C5, C6 or C9 (only up to C9 (∆ delta)).

Linoleic acid 18:2c∆9,12 or linolenic acid 18:3c∆9,12,15 cannot be synthesized as they require desaturation beyond C9. These must be provided in diet: Thus are Essential Fatty Acids

Omega 6 (n-6) (means the first double bond is 6C from the terminal CH3):Linoleic acid (C18:2)Gamma Linolenic acid (C18:3) = GLAArachidonic acid (C20:4)

Omega 3 (n-3) (means the first double bond is 3C from the terminal CH3):Alpha Linolenic acid (C18:3) ALA PlantsEicosapentaenoic acid (C20:5) EPA FishDocosahexanoic acid (C22:6) DHA Fish

EPA and DHA melting point = -54°C!

Omega-6 Omega-3Gamma-linolenic (GLA) Alpha-linolenic ALA

↓ ↓↓ ↓

Arachidonic acid EPA↓ ↓

PGE2 DHA↓ ↓↓ PGE3

Inflammatory Anti-inflammatory

EFA: Need as 1% of calories

WHO/FAO: omega 6 : omega 3 PUFA ratio from 4:1 to 10:1

Deficiency omega-6: Reduced growth, reproduction Skin lesions, dermatitis, impaired wound healing Edema, subcutaneous hemorrhage Reduced Inflammatory response

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ALA conversion to EPA is not efficient. At best about 10% is converted. A lot of flax oil can be added – then you can say theres a lot of omega-3s but you don’t know the actual conversion that can be used. If you buy fish oil it contains mostly EPA and DHA. Problem: these FA’s can be easily oxidized (and make it NOT biologically active).


You want both in a balanced diet.


Crystalize below -54 – so its protective for these fish at very low cold tempereatures.


Found in COLD water fish.


Grasses, walnuts, flax- canola- soy oil.


These 3 are all essential fatty acids! Too much Omega-6 is pro-inflammaatory to the immune system (BAD) They are essential for healthy skin (GOOD). All about proportion consumed.


Essential because we don’t have FA desaturase that works beyond carbon 9.


Desaturates F.A (makes them unsaturated). If we need unsaturated F.A past C9 then we need to get them from the diet.

Mechanisms of action for omega 3 FAs: Anti-arrhythmic Anti-thrombotic Anti-atherosclerotic Anti-inflammatory Improved endothelial function (vasomotor function/dilation) Lowers blood pressure Lowers triglyceride level

Aspirin: "non-steroidal anti-inflammatory drugs" (NSAIDs) (aspirin, ibuprofen,

acetaminophen) inhibits the synthesis of prostaglandins from

arachidonic acid

Some important fatty acids of refined vegetable oils in Canada (w/w %)

Fatty Acid

Flax Canola Soybean Corn Peanut Sun-flower

Olive Palm

16:0 6 4 9 11 11 7 14 4218:0 3 2 5 2 3 5 2 418:1 17 55 45 27 46 19 64 3818:2 16 26 37 59 29 66 16 918:3 56* 10* 3* 1 1 Tr Tr20:1 2 Tr Tr Tr Tr Tr22:1 Tr Tr Tr Tr

* α-linolenic acid (omega 3) Fish oil, flax, canola/rapeseed, walnuts, soy sources of α-linolenic acid

Canola oil positive factors: High in C18:1;LA (omega 6) : ALA (omega 3) = 2:1

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Flax: 56% ALA – if you want omega 3 fatty acids – you consume flax oil because its LOADED with ALA. Whats the concern when you have lots of C18:3 unsaturated FA – oxidation damage leads to the development of rancid fat. Canola Oil: has 10% ALA, 26% linoleic, and 55% oleic acid. It is a “heart healthy oil” because the composition is almost ideal in terms of preventing coronary disease. This is because of the ratio of (18:1 : 18:2). It also has some omega 3 FAs Soy oil, corn oil, peanut oil is not quite as good as canola oil. Palm oil – Has fair amount of c16:0 – is much more saturated like (is hard/solid). Olive Oil is 56% C18:1 (oleic acid).


NEED TO UNDERSTAND THE DIFFERENT PROPERTIES OF THE OILS – KNOW STRENGTH AND WEAKNESSES (OLIVE OIL, CANOLA). Not much oil/fat used in animal nutrition – but we do add some to their feed. The max amount of oil in a ruminant is about 7% - above this would kill all the rumen microbes. We do add some fat because its energy and has a lot of calories. Unsaturated FAs (canola) to pigs – you get an “oily” kind of carcass. Lots of keratine in corn oil (gives it a yellow colour) – consumers do not like yellow fat. Barley and Wheat gives the carcass nice hard fat. Not much canola because then you get oily fat in the carcass.


Inhibit the production of PGE2 (prostaglandins) from Arachidonic Acid (in the omega-6 pathway). This shifts the omega-6 omega-3 ratio.


These are all positive claims. But in science this is not exactly replicated so we do not necessarily trust this.

Health Canada Diet Target ω 6 : ω 3 = from 4:1 to 10:1

US: 2.5 : 1 as ideal; 250 mg/d (2011)Common: 20:1(HUMAN DIET)

Ratio more important than absolute amounts

Essential fatty acids for cats and dogs

Essential fatty acid (g)

Growing puppies allowance (per kg BW0.75)

Adult dogs recommended allowance (per kg BW0.75)

Bitches late gestation and peak lactation allowance (per kg BW0.75)

LA 0.8 0.36 1.6ALA 0.05 0.014 0.10AA 0.022EPA + DHA 0.036 0.03 0.06

Essential fatty acid (g)

Kittens allowance (per kg BW0.75)

Adult cats allowance (per kg BW0.75)

Queens late gestation and peak lactation allowance (per kg BW0.75)

LA 0.29 0.14 0.3ALA 0.01 0.011AA 0.01 0.0015 0.011EPA + DHA 0.05 0.0025 0.0044

Source: Nutrient Requirements of Dogs and Cats. 2006. National Research Council (U.S.)

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SEE supplemental slides for more information about FA’s –and their structures, health benefits, etc. Corn oil, Safflower Oil, Sunflower Oil – are high in omega 6’s Flaxseed oil, canola oil, soybean oil, are high in alpha-linoleic acid.


Because there are some shared enzymes within the two pathways: omega-6 omega-3

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Feed an animal triglyceride – and lipases will breakit down into FFAs and glycerol. Only the glycerol is utilized within the ruminant fermentation acid to form maily proprionic acid with some butyric acid. FFAs not used by rumen microbes. The only thing the microbes will do is hydrogenate the unsaturated fatty acids and form some trans fatty acids. The FFAs attach to feed particles and then move through the gut and are absorbed in the small intestine (similar to a monogastric animal). Bypass Fat – fat moves through the rumen in tact until it gets into the SI where it is digested like a monogastric animal.

Fatty acids are not a source of energy for microbes.

Minimal degradation of long-chain fatty acids in the rumen.

Long chain fatty acids not absorbed from the rumen (VFAs are)

Active hydrogenation of unsaturated fatty acids

Microbial synthesis of long-chain fatty acids in the rumen (15g/kg nonfat org matter fermented)

More fat leaves the rumen than is consumed by the animal

Lipids leaving the rumen:

80 to 90% free fatty acids attached to feed particles and microbes About 10% microbial phospholipids Some undigested feed fat bypasses rumen

Diagram of the molecular structure of different fatty acidsSaturated fat Cis-unsaturated fatty acid Trans-unsaturated fatty acid

saturated carbon atoms (each with 2 hydrogens) joined by a

single bond

unsaturated carbon atoms (each with 1 hydrogen) joined

by a double bond. Cis configuration.

unsaturated carbon atoms (each with 1 hydrogen) joined

by a double bond. Trans configuration.

Oleic acid (C18:1 cis 9) Elaidic acid (C18:1 trans 9)Oleic acid is a cis unsaturated fatty acid that

comprises 55-80% of olive oil.Elaidic acid is a trans unsaturated fatty acid often found in hydrogenated vegetable oils.

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Hydrogenation – get the formation of trans bonds. If you have a cis bond – you get kinks in the FFA tail – then you get a lower melting point – and increased fluid development. Trans FA – you barely get kinking in the tail. Research showed that physiologically this TFA behaves like a saturated fatty acid – in fact its even worse than a SFA. People were told to eat margarine instead of butter. But the margarine had lots of trans fatty acids – actually worse than the saturated FAs found in butter. Then the margarine companies had to switch up their formula to have less TFAs (Becel – expensive).


Microbe membranes

http://en.wikipedia.org/wiki/Elaidic_acid

http://en.wikipedia.org/wiki/Oleic_acid

http://en.wikipedia.org/wiki/Image:Fat-Conformation-Sat.gif

http://en.wikipedia.org/wiki/Image:Fat-Conformation-Cis.gif

http://en.wikipedia.org/wiki/Image:Fat-Conformation-Trans.gif

These fatty acids are geometric isomers (chemically identical except for the arrangement of the double bond).

Trans fat not usually present in food unless use of hydrogenation process of PUFA

oils high trans fat content. Small amounts of trans fats found in ruminant

produced food (rumen microbial hydrogenation)

Conjugated Linoleic Acid (CLA) Present in ruminant fat, and produced in rumen fermentation by microbial

saturation of UFA

Linoleic acid (cis-9, cis-12 C18:2) hydrogenated to several trans forms

including CLA (cis-9, trans-11 C18:2)

POSITIVE HEALTH EFFECTS OF CLA - A novel nutraceutical o Anti-carcinogenic

o Anti-atherogenic

o Anti-obesity (nutrient partitioning)

o Enhanced immune system

o Prevents or delays diabetes

Milk fat contains 3.5 to 7 mg CLA/g fat

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A trans-fatty acid that is actually good for your health. It is produced in the rumen and is found in milk fat. Cis 18:2 hydrogenated to CLA.

http://en.wikipedia.org/wiki/Geometric_isomer

http://en.wikipedia.org/wiki/Image:Oleic-acid-3D-vdW.png

http://en.wikipedia.org/wiki/Image:Elaidic-acid-3D-vdW.png

http://en.wikipedia.org/wiki/Image:Oleic-acid-skeletal.svg

http://en.wikipedia.org/wiki/Image:Elaidic-acid-2D-skeletal.png

CLA content in some foods

Food CLA isomers cis 9, trans 11mg/g fat %

Beef 4.3 85Pork 0.6 82Chicken 0.9 84Milk 5.5 92Colby cheese 6.1 92Corn oil 0.2 39

Increasing CLA isomers in foods produced by ruminants: Grass pasturing

Feeding unsaturated vegetable oils: fish oil, flax oil, canola oil.

Can increase CLA content from typical 3-4 mg CLA/g fatty acids to 5-25 mg in

milk.

Feeding unsaturated oils with high concentrate diet (low rumen pH) trans-10,

cis 12 CLA isomer inhibits milk fat synthesis low milk fat

Effects of Fats on Rumen FermentationUpper limit is around 7-8% fat in diet. Typical is about 3% fat in diet ingredients and

then one can add up to 3% from a fat source.

Lipid-coated feed particles: interferes with attachment of microbes and enzymes to

feed

Cytotoxic to rumen microbes (cell membranes):

FA associate with cell membranes masking cell membrane receptors and

enzyme secretion

Become incorporated in cell membranes and changing fluidity (electrolyte

transport)

PUFA may change redox conditions in cells, oxidation stress

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Ruminant fermentation system not capable of handling a large amount of fat. So feeding canola oil can be bad if you feed too much. When you feed canola oil and concentrates: High C18:2 and low pH can produce more bad trans fatty acids and inhibit the synthesis of milk fat in the mammary gland. Cannot feed ruminant more than 7-8% of their diet as fat!


Grass has a lot of C18:2. Feed ruminants canola or flax oil – to get more CLA in the milk.

- PUFA oils are more inhibitory than saturated fats

- Feeding whole oil seeds with high PUFA content less inhibitory due to

lower availability

Consequences:

Reduced feed intake

Reduced fiber digestion! (reduced fermentation activity) Reduced milk fat

Increase propionate/acetate ratio

Fatty acids can be used to defaunate the rumen (protozoa very sensitive)

OXIDATIVE RANCIDITY

Auto-catalytic reaction in unsaturated fatty acids with generation of oxygen

radicals and potentially leading to spontaneous combustion

Accelerated by pro-oxidants

• Heat

• U.V. Light

• Moisture

• Transition Metals eg Cu, Fe, Mn

Anti-oxidants

• Vitamin E (& A)

• Ethoxyquin (synthetic Vit E)

• Butyl Hydroxy Anisole (BHA)

• Selenium glutathione peroxidase

Cholesterol:Many important steroids are derived from cholesterol in animals, including:

HORMONES including androgens, estrogens, progestins, glucocorticoids, and mineralocorticoids

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These clean up the radicals that are generated.


These compounds prevent oxidation from occurring!


Electron donors that drive these redox reactions that involve these radicals. If you have oil with a transition metal contamination it is very hard to stop oxidation reaction from happening.


Positively feedback on themselves and oxidizes more molecules to create more oxygen radicals. This can lead to spontaneous combustion!


Kills all the microbes.

BILE ACIDS which are detergent molecules secreted in bile from the gallbladder that assist in the absorption of dietary lipids in the intestine

Animal products are a source of cholesterol- important in human nutrition

Normally not considered in animal nutrition as the diets are mostly made up of plant ingredients

WATER

Sources (3): Drinking water Water in feed (Eats). Metabolic water

Functions of water: Solvent GIT extra- and intra-cellular and for excreta Chemical reactions – Synthesis of urea, protein hydrolysis Lubricant and solvent for lubricants Temperature regulation Physical protection, cushions organs and nerve tissue

Average daily water requirements

Class of livestock L/day Dairy cow 160Beef cow 55Beef steer 35Feeder pig 7-10Ewe 2-7Laying hen 0.25

Water content of feeds:

Feed % waterCorn 12Barley 11Oats 9Hay 10 (8-15)Silage 70 (45-75)Beets 87Potatoes 75

Metabolic water formed from:

Carbohydrate 60%Protein 40%

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Root crops are high in moisture content. If you have a cow eating a lot of hay you will need to supplement water. If you feed them silage you will still need to give them water – just less.


Changes in response to environmental stressors: temperature, etc.


Water is important because it varies a lot in quality and comes from many different sources. We don’t really have a water reserve this is why we need to drink it on the daily.

Fat 100% (1 g water per 1 g fat)

Factors affecting water requirement:

DM intake. Water intake is 3x DM intake Composition of feed. Increased by salts and minerals Physiological state: lactation, pregnancy Ambient temperature and relative humidity (RH) Temperature of drinking water Frequency of watering. Most species require at least 3/day or DM intake is

reduced

Water quality

Good water: Clear and colorless Low total solids No disease organisms, pesticides No undesirable flavour or odor No objectionable gases

Quality considerations TDS = Total dissolved solids, mg/L

Hardness: Soft water = <60 mg/L Ca + MgVery hard = >800 mg/L Ca + MgMaximum for livestock = 1000 mg/L

Salinity: (salts, mainly NaCl) estimated from conductivity (EC) and may be expressed as TDS mg/L

TDS EC<1000 <1.5 Excellent for all types of livestock

1000 - 3000

1.5-5 Satisfactory for all livestock but may slightly reduce productivity, mild diarrhea, especially poultry

3000 – 5000 5-8 Acceptable except poultry. Will cause temporary diarrhea and may be refused at first

5000 - 7000 8-11 Usually safe for beef cattle, sheep, swine and horses7000 – 10,000

11-16 Not suitable for young, pregnant or lactating animals

>10,000 >16 Not recommended under any conditions

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Poultry are sensitive to water quality. Poor water quality can also reduce milk production.


Soft water is low in calcium/Mg – very hard water is very high in calcium/Mg.


Tells you how “dirty” the water is – with dirt, sand, clay, microbes, manure, etc.

Livestock water quality guidelines

Parameter mg/L (maxima) = PPM Calcium 1000Nitrate + nitrite 100Nitrite alone 10Sulfate 1000TDS 3000 (2000 for aquatics)

Aluminum 5Cadmium .02Copper 1 (cattle)

0.5 (sheep)5 (swine and poultry)

Fluoride 2Lead .1Mercury .003Molybdenum .5Selenium .05Zinc 50

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Common water quality problems

Sulfate >1000 mg/LSource: Calcium sulfate rock (gypsum)Effects: Reduces availability of Ca, Zn, Fe, Mn, Mo, CuAction: Improve water quality and/or provide additional trace minerals,

especially Cu

Nitrite > 10 mg/L OR nitrate + nitrite >100 mg/LSource: Fertilizer or animal wasteEffect: Formation of methemoglobin (brown blood), reduced vitamin A

utilization and absorptionAction: Prevent contamination

Iron > 2 mg/LNot a nutritional problem. Causes scale formation in pipes; may form slimy bacterial films, poor taste.Can chlorinate and filter to remove iron

Fecal contamination:Coliform count should not exceed 10 CFU/ml.Cryptosporidium, enterotoxigenic E. Coli, Salmonella, Leptospira, protozoa, round worms

Biochemical Oxygen Demand (BOD):

Organic content of water - Chemical measure for estimating the amount of dissolved oxygen needed by aerobic biological organisms in a body of water to break down organic material present in a given water sample at a certain temperature over a specific time period.

BOD of 3-5 mg O2/L water is maximum for aquatic life. Poor taste at 1-3 mg O2/L water

Blue-Green Algae (cyanobacteria): Unpalatable and may contain toxins

Suggested water treatments:Problem SolutionColiform count Chlorinate waterWater hardness Install softenerHigh nitrates or other minerals Ion exchange or RO systemIron FiltrationHigh water pH AcidificationHigh turbidity Coagulation

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Vulnerability of water supplies

1. Surface water2. Cisterns3. Natural springs4. Shallow hand-dug or sandpoint wells (<50 ft)5. Artesian wells6. Drilled wells7. Public water supplies

Small Animals

Water requirement for dogs and cats is linked to energy consumption (water : calorie ratio).

Water (ml per day) : ME (kcal per day) = 1 : 1

Dog example: 10 kg adult dog Maintenance requirement is

132 x BW0.75 = 742 kcal ME Water : energy ratio is 1:1 Water requirement = 742 ml Of that 742 ml about 74-119 ml is generated from metabolic water. Required water intake from water and feed then is ca. 642 ml per day.

Cats: Same ratio, but it is recommended to double the volume to allow for lifestage, environment, work activities.

For both cats and dogs the recommendation is to allow animals to self regulate as opposed to working with required intake of water.

Protein Nutrition

1. Introduction, general, classes of proteins, amino acids

2. Non-ruminant protein nutrition a. Quality:

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i. Protein digestibility: ileal vs. fecal Amino acid digestibility: ileal vs. fecalAmino acid balance, biological valueAssay for protein quality

b. Requirement:i. Maintenanceii. Production

3. Ruminant protein nutrition a. Versus non-ruminantb. Microbial fermentation:

microbial protein synthesisfrom non-protein nitrogen (NPN)energy interaction

quality of microbial proteinc. Feed protein:

Solubility of NDegradable protein Bypass protein

Protein:

1. Primary function : Source of amino acids for body protein orsource of Nitrogen for ruminants

2. Secondary function :Source of energy during: - consumption of excess protein - consumption of poor quality protein

Lower efficiency of energy utilization (only 70-75 % vs carbohydrate 95%) due to energy cost required for clearance of NH2

Urea cycle and uric acid production require energy

Protein nutrition is complex:

chemistry (23 amino acids)more metabolic pathwaysessential vs. non-essential amino acidsdifferent digestion coefficients between amino acidsrelative proportions of amino acids in feed matteroptimal relative proportions of amino acids change with physiological state

(growth, lactation, pregnancy, disease)very limited storage of amino acids

Protein turn-over g / day:

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Protein intake represents only 1/3 of total protein synthesis

Human: intake 100 g/dgut secretion 70 g/d

170 g/dfecal loss 10 g/dabsorbed 160 g/d

Protein turn-over:

Protein synthesis / day 300 gProtein intake / day 100 gAmino acids re-used daily 200 g

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Protein:

highest concentration in muscle (apart from water) important in tissue growth animals have limited ability to synthesize protein: from amino acids only, and

not from NH2

of all nutrients protein deficiency or imbalance between amino acids has the most pronounced negative effect on carcass quality

Conclusion: Protein is an essential component in the diet.

Forms of proteins:

1. Fibrous : collagen, elastins, keratins2. Globular : albumins, globulins, glutelins, histones, prolamines, protamines3. Conjugated : nucleoproteins, mucoproteins, glycoproteins, lipoproteins,

hemoproteins, metalloproteins4. Derived : poorly defined, product of degradation

Amino acids:

Primarily used in the L- form, with a few exceptions Some OH analogs may substitute such as methionine hydroxy analog. Done for

economic reasons.

Use of D and L amino acids by non-ruminants:

Amino acid D form relative to LMET (hionine) =PHE (nylalanine) =PRO (line) =LEU (cine) < slightlyVAL (ine) ½TRY (ptophan) limitedISO (leucine) limitedHIS (tidine) limitedLYS (ine) 0 (negative effect)THRE (eonine) 0ARG (inine) 0

Classification of amino acids:

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Essential (EAA; 10) Non-essentialArg (inine) Ala (nine)His (tidine) Asp (artic acid)**Iso (leucine) Cys (teine)Leu (cine) Gly (cine)**Lys (ine)* Ser (ine)Met (hionine)* Tyr (osine)Phe (nylalanine) Pro (line)**Thre (onine)* Glu (tamic acid)**Try (ptophan)Val (ine)

* Not present in adequate quantity in grains** Essential in some cases or may have non-nutritional effect (functional food)

Cats (carnivore): Taurine is an Essential AA (present in meat)

Specific amino acid relationships:Methionine: Requirement only met by MetCysteine: Requirement met by Cys or Met

Phenylalanine: only met by PheTyrosine: met by Tyr or Phe

Gly and Ser: interchanged

Protein analysis:

Normally Crude Protein (CP) Uses the Kjeldahl procedure and is a measure of total N in sample.

o Non-protein nitrogen (NPN) is also converted to N and measured as N

Use Kjeldahl factor to determine protein based on N being constant in feeds at 16 % of total protein (100/16 = 6.25)

The factor can differ between some foods (milk = 6.38; feed = 6.25)

Amino acid analyses are used mainly in research and by feed companies for quality control. Expensive and not used in routine ration formulation.

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Phe can be metabolically converted to Tyr.


Met can be converted metabolically into cysteine.


Can act on the pituitary gland and cause it to release more growth hormones. Increased muscle mass and bone density.

Monogastric protein nutrition(pigs, poultry, cat, dogs, humans)

Protein quality measurements:

Digestibility:

Apparent: P intake - P outputP intake

True: P intake - (P output - MFP)P intake

MFP = Metabolic Fecal Protein = MFN x 6.25MFN = Metabolic Fecal Nitrogen

MFN is determined by:1. Feeding a protein free diet and measure N in feces.2. Feed different levels of protein in diets, measure N in feces, and extrapolate

N back to a 0% protein diet.

Does not work in poultry because urine contaminates the feces

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Represents the true digestibility. It is corrected for the amount of protein that was not of feed origin (endogenous protein).


How much protein consumed – protein lost in feces. With these equations you make the assumption that the protein left over is actually absorbed or was it a useful A.A.

Digestibility of protein is affected by a wide range of factors:1. Heat damage of protein (enzymatic browning or Maillard reaction: formation of

aminosugar complexes (Lys)).2. Level of feed intake.3. In forages age of plant at harvest (% fiber).4. Anti-nutritive factors:

- Trypsin inhibitor in raw soybean- Gossypol interferes with Lys- Lectins interfere with amylase- Tannins are complexing agents

Which method of measuring digestibility is more reliable to estimate true nutrient absorption?

Use composition of the feces or of the digesta at the ileal-caecal junction (Ileal vs. fecal method)?

Consider interference by fermentation and metabolism in the caecum and large intestine:NH3 is generated, absorbed into the blood stream and excreted in urine

Remember that digestibility measures disappearance of N or protein (N x 6.25) from the G.I. Tract and not absorption)

Example: Sorghum protein for pigs

Ileal Fecal Apparent digestibility % 60.4 71.1True digestibility % 69.0 78.4

Does CP digestibility reflect digestibility of all amino acids in the crude protein? No

Use ileal or fecal method for estimating digestibility of amino acids? Ileal method.

True digestibility AA (%) Ileal Fecal

Lysine 73.4 77.8Methionine 77.6 76.5Phenylalanine 71.5 81.1Valine 72.6 80.2

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Best method to use to access true digestibility.


Corrected for MFN. The digestibility in the illeal is always lower than the fecal method of analyses. In fecal 71.1 and illeal 60.4 – so around a 10% loss – which means 10% went to the cecum/LI and was converted to ammonia and eventually excreted in urea.


When you sample this way you take before the digesta passes through the cecum (large intestine). In cecum/LI – receives any undigested protein – and microbes will break it down – end product is ammonia – which crosses the intestine and into the blood – even though its totally useless to the host – they don’t use it for anything they just excrete it.


Trypsin starts out the entire protein digestion system – so you do not want to inhibit trypsin. Soybean meal has usually been heat treated to denature the trypsin inhibitor and makes it NOT biologically active. If you denature trypsin inhibitor you also will denature the high quality amino acids/proteins in the soymeal.


Ties up lysine – not biologically available (also #1 limiting EAA in our diets). Two examples of enzymatic browning: When you fry an egg and theres a bit of brown around the egg white. When you bake bread and the outside gets brown. Also contributes to good smells. Like in a bakery when you like the smell of fresh bread.

Example of fecal vs. ileal measurement

Comparison of ileal and fecal digestibilities of raw and heated soybean meal (SBM) (heat treatment inactivates the trypsin inhibitor in soybeans)

Raw HeatedFecal Ileal Fecal Ileal

Lys 71.9 44.2 87.3 84.9Met 61.0 46.7 82.5 83.0Cys 77.7 35.2 87.0 74.1Thr 65.2 32.2 83.0 71.5Tryp 75.4 24.8 86.8 72.3

Are amino acid digestibility’s constant for each feed or do they change with different feeds used in a feed formulation (matrix effect of ingredients)?

Not constant due to matrix effects.

Protein quality - Amino acid balance in feed

= concentration of amino acids in feed in relation to physiological needs: growth, lactation, pregnancy, eggs, wool

Close match high quality proteinPoor match low quality protein

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Is an amino acid deficiency = poor quality protein – there is a tendency to see the protein deposited as fat instead of muscle.


If you need a certain amount of lysine and the protein supplies that need and is not less than the need then it is a good protein quality.


Very important concept that needs to be understood!


SI is responsible for the absorption of AA – some will go into the liver – undergo urea cycle – blood ( kidneys ( excreted as urea in urine. If theres lots of urea showing up in the urine afer being fed there are poor quality protein/AA in the diet. Undigestible protein winds up in the cecum and then the large intestine. It consists of undigested feed protein, MP (microbial protein), and MFP (metabolic fecal protein). Because of fermentation you’ll find that when the microbes degrade the protein in cecum/LI and they break it down into ammonia then they synthesize de novo A.A. There is a loss of ammonia that crosses the wall of the hind gut ends up in the circulation. We know how much protein disappears but we do not know what is is absorbed as and if it was actually useful for the host.


They are not constant because other compounds in the feed can interact with how the amino acids are digested.


Heat treated to inactivate the trypsin inhibitor. Most of the amino acids are very digestible in the commercial heated soybean meal.


The trypsin inhibitor is present in the raw feed (which reduces the digestibility of protein).


This shows that raw soybean meal has a much lower digestibility compared to the heated soybean meal.

Deficiency of 1 amino acid will stop protein synthesis. Animal uses protein for energy and fat synthesis. Some will be cleared as urea/nitrogen in the urine.Which could signify that the animal is getting too much protein or a protein of poor quality.

Identify limiting amino acid(s) in poor quality protein. 1st, 2nd, 3rd

Poor amino balance growth response to the addition of limiting AA.

Ie. Zein (corn protein) - poor quality- growth –ve

Growth in rats fed zein, or zein supplemented with tryptophan or with tryptophan and lysine

Osborne and Mendel 1914

Lys 1st limiting; tryp 2nd limiting

1. Aim for an ideal balance of A.A. in the feed.- match with what is digested from the ileol-cecal method.2. Fast growth ---- lean tissue amino acid composition is the requirement.3. Ideal protein concept

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When feeding zein animals were losing weight and would eventually die. They susrpected tryptophan was lacking so they added it and it slightly reversed the weight loss of the animal – however animals still not doing great. This means tryptophan was not the 1st limiting A.A. They then added lysine along with tryptophan then there was a steep increase in growth. The concluded that lysine was the 1st limiting AA and tryptophan was the 2nd limiting AA.


Animals will not survive on zein.

Measuring protein quality

1. Ideal protein = ideal AA pattern concept

Liebig’s “Law of Minimums"

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Feed increasing levels of lysine – each time you add a bit more you get a weight gain response in the animal. Eventually you will hit a plateau. When it starts to plateau – is the indicator of how much A.A are needed in an animals diet.

Undersupply of one single essential amino acid will inhibit the use of those in adequate supply

Ideal protein:

Established ideal pattern (balance) of digestible essential amino acids for lean meat deposition (protein accretion), when supplied with sufficient nitrogen for the synthesis of non-essential amino acids.

No excess, no deficiency and as little conversion of amino acids for energy is desirable. N excretion is minimized.

The assumption is that the pattern of amino acids required does not change relative to the amount of lean tissue deposition, but the absolute amount of amino acids or ideal protein required does.

The level of individual amino acid required is expressed on a ratio basis to lysine, which serves as the reference amino acid.

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Rain barrel concept. All A.A. are in sufficient supply. Protein synthesis will go up until what the 1st limiting amino acid will allow. (dotted line on the rain barrel) above the line all the protein will be de-aminated. Similar concept.

Lysine is 1st or 2nd limiting amino acid. Simple chemical analysis in feeds. Lysine is used primarily for protein accretion. A lot of information on lysine requirements is available. Synthetic lysine is cheap

Ideal Protein:

Is a perfect balance of amino acids that will cover the requirement of the animals

Lysine is always set at 100% - all other amino acids are set as a % of lysine Allows for the calculation of the requirement of all amino acids if the lysine

requirement is known

2. Biological assays

Protein Efficiency Ratio (PER) - dates back to 1919:

Feed efficiency measured on a protein level basis 10% CP in ration, 28d period Reference protein is casein Measure g gain/g protein consumed Rats or chicks

Quality is measured in terms of growth only, not great for lactation or pregant animals. More applicable to children. Used in human nutrition and is a simple and cheap testing method.

The test is highly standardized by WHO. Standard reference casein available for PER tests.

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If protein has an A.A deficiency (1st, 2nd, 3rd limiting A.A) – you get an increase in growth but then it plateaus. At plateau feeding at more than the requirement (when you feed more of a substance that’s low in certain A.A the animal can eat more to get their required levels).


Still used today in developing nations.

Nitrogen BalanceTrue Biological Value: NI – (FN - MFN) – (UN - EUN) x 100

NI – (FN – MFN)

Measures N retained as a % of N absorbedClassic test

Biological value of proteins for growing and adult ratsProtein Growing Adult

Egg albumin 97 94

Beef muscle 76 69

Meat meal 72-79 -

Casein 69 51

Peanut meal 54 46

Wheat gluten 40 65

Many other tests including: Available lysine (color reaction) to test for Maillard reaction products In vitro (testubes) to simulate protein digestion

Feed Protein for Ruminants:

Quantity: The quantity of protein to be fed depends on the protein requirement of the ruminant and on the quality of the protein in the feed.

Quality of Protein for Ruminants:

Digestibility: Traditional method which has limitations as discussed. Digestibility of protein in forages is lower than that of grains and protein supplements.

Forage protein digestibility depends on:

- Forage species- Forage maturity- Weathering- Heating (Maillard reaction)

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In ruminants youre dealing with forages which is harder to digest than grains.


Non-ideal A.A composition – low on lysine, methionine, and one other is deficient – which lowers the biological value of the feed.


Almost half of the A.A protein were retained in the body and about half was excreted in the urine. What was absorbed!! Not what was eaten.


Very high quality protein – 97% of nitrogen was absorbed and contained w/in the body and only 3% appeared in the urine.


Nitrogen lost in the urine as a percent of what has been absorbed. Is a measure of true protein digestibility and measures the retention of the nitrogen. NI = nitrogen intake FN = fecal nitrogen MFN = metabolic fecal nitrogen (from endogenous origins) UN= urinary nitrogen EUN= endogenous urinary nitrogen (nitrogen derived from endogenous sources – has nothing to do with the feed)

Modern protein classification based on:

1. Solubility in rumen:Totally and fast degraded to NH3

True protein and NPNDetermined in buffer

2. Undigestible N (bound protein): ADF-bound; perform N assay on ADF

3. Degradability in rumen:Protein to varying degree is broken down to NH3. The rate of breakdown depends on physical characteristics of the protein, and on physical conditions in the rumen (passive/dilution rate).Measured by protein disappearance from porous nylon bags hung in the rumen of fistulated ruminants.

4. Bypass protein (escape/undegradable):The protein is not broken down in the rumen and arrives in the abomasum intact. Measured by nylon bag technique. Useful to target limiting amino acids to the S.I., and also to increase total protein available to high producing ruminants.

3. RUMINANT PROTEIN NUTRITION 1. OPTIMIZE MICROBIAL PROTEIN OUTPUT

2. OPTIMIZE BYPASS PROTEIN / FEED PROTEIN TO MEET NEEDS OF

THE ANIMAL

3. MINIMIZE LOSS OF NH3 (COST AND BAD 4 ENVIRONMENT)

3.1 MICROBIAL PROTEIN :3.1.1 QUALITY

REL UNAFFECTED BY DIET

Biological Value = 80% (BACTERIA + PROTOZOA)

TRUE DIGESTIBILITY:

PROTOZOA 88%

BACTERIA 66%

PROTOZOA ON ROUGHAGE DIET

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Single cell proteins.


Relatively constant – can’t really change it by changing the diet. If you feed more roughages then you get more protozoa that have higher protein quality. Microbial protein is a good quality protein – better than grain protein, but not as good as high quality animal protein.


0% degradable – Undegradeable. Escape = escapes fermentation and escapes being converted into ammonia. Remains completely intact.


Measure of how quickly the feed digesta moves through the rumen abomasum, SI, LI. Test feed stuff in porous nylon bags – hang them into the rumen – remove a bag every 30% so you can construct a fermability/digestibility curve for a certain feedstuff.


Protein in rumen – broken down to ammonia some is not converted. It will travel through the digestive tract and stay in its same original form. Some feed is more degradeable, some is not. Canola protein is 60% degradable ( 60% will be converted to ammonia. 40% will pass through the GI in its original form.


Undigestible protein in a forage – can be determined chemically – this is the nitrogen associated with the ADF fraction – undigestible.


Is a measurable parameter. How quickly and completely a protein is degraded to ammonia. This means it can be non-protein nitrogen (urea), or true protein. Solubility is fixed. There is 100% certainty that solubilized nitrogen will be broken down to ammonia.

20% NUCLEIC ACIDS

INFERIOR TO HIGH QUALITY ANIMAL PROTEIN

SUPERIOR TO GRAIN PROTEIN

EQUAL TO SOYBEAN MEAL OR CANOLA MEAL OR ALFALFA

NB SOYBEAN MEAL = SBM

CANOLA MEAL = CM

RAPESEED MEAL = RSM

3.1.2 QUANTITY OF PROTEIN SYNTHESIS IN RUMEN by microbes1. INHERENT METABOLIC LIMITATIONS IN BACTERIA AND PROTOZOA

2. PHYSICAL LIMITATIONS: SIZE OR CAPACITY OF RUMEN; FLOW OF

DIGESTA

3. ENERGY SUPPLY FOR PROTEIN SYNTHESIS; OTHER NUTRIENTS

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The more energy provided – the more protein synthesized by microbes in the rumen.


How big is the rumen? “How large is your tank”. The bigger the rumen the more microbial growth. Think of the rumen as a continuous fermentation system. Products constantly moving in and out. The higher the flow rate and the more quickly you remove the end products the higher the growth of microbes will be. If flow declines there is a lower production of microbes in the system.


They can only make so much protein!

Super Important Figure to Study for Exams.

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IMPORTANT TO STUDY!!!! 100% of NPN is converted into ammonia. If you take a true protein –about 60% of the protein is broken down to ammonia and 40% of the protein bypasses rumen fermentation system and moves into abomasum/SI. The ammonia picked up by microbial fermentation system and causes growth of microbes! Microbes will eventually move down the rumen, abomasum, to SI, LI and is eventually digested in a way that a monogastric animal would. Absorbed a lot in the ilium. How much of the ammonia will be picked up by microbes? It is driven by how much fermentable energy (TDN) the animal has. High TDN = high grown and more microbial protein. Low TDN = less microbial growth ( still have ammonia present – starts building up – overflows than crosses rumen wall and enters circulation ( liver ( urea cycle ( urine (is a lost source of nitrogen – costs energy to excrete the nitrogen). Overflow ammonia may also end up in the saliva that will eventually flow back into the rumen. Moose are on protein/energy deficient diet in the winter – the wild ruminant will start losing body weight (mobilizing muscle and adipose tissue). Muscle protein broken down, deamination occurs, produces an amino group that winds up in the liver and is converted to urea which is then shunted back into the rumen via saliva.

Factors affecting the amount of microbial protein synthesis

1. Rumen nh 3 concentration

Max rate and efficiency of microbial protein synthesis is

at 5 mg nh3 /100 ml rumen fluid

> 5 mg / 100 ml nh3 to blood liver urea loss

< 5 mg / 100 ml n lack

2. Rumen pH pH high nh3 diffusion

pH low nh4 + slow diffusion

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Prior to feed – ammonia deficit. Feed the animal and you get an excess of ammonia (over 5%) – extra is lost. Period between feedings is also a lack of ammonia. The animal fed for the second time and ammonia increases. How do you get it closer to 5% throughout the day? Feed the animal more frequently – you get less excess and fewer deficiencies over time. 30 years ago farmers fed the cattle in a similar way as the top graph – 2x a day – may be one of the reasons milk production was low (~6000 mL) compared to 12000 mL of today.


High pH means more ammonia is lost across the rumen wall. pH low (H+ high) and binds to NH3 ( NH4 and less is lost across the rumen wall. The lowest pH that we allow in the rumen is 5.5 – when eating a forage diet pH is around 6.5


Want to keep it around 5%

3. DIETARY ENERGY LEVEL (need energy to drive microbial growth)

Microbial Protein % TDN Produced g/KG DM

> 75% 51.265-75% 38.4< 65% 26.0

UPPER LIMIT OF NON PROTEIN NITROGEN UTILIZATION WHEN

SUPPLEMENTING UREA (FERMENTATION POTENTIAL)

% PROTEININ RATION % TDN (DM)BEFORE NPN IS ADDED

60-65 65-70 70-75 75-80

MAX CP AT WHICH NPN IS USED8 % 10 10.5 10.9 11.210 % 10.8 11.3 11.7 12.0

This example suggests that 3.2 % crude protein can be added in the form of urea

when the starting CP is 8% and at 75-80 % TDN. If more is added, the NH3 from

urea will be lost in urine as it cannot be used by microbes

UREA FEEDING RULES: Urea contains 45% N, thus 1% urea contains 45/100 X 1 X 6.25 = 2.81 %

crude protein.

LIMIT 1% OF GRAIN MIX; 0.5% TOTAL DIET

UREA IS NOT PALATABLE, MIX IN FEED WITH MOLASSES

4. RATE OF FERMENTATION OF CARBOHYDRATE

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Has neurotoxic effects when over fed that may lead to death – this is why we do not add more than 1% urea to their diet.


Cheaper – but it is extremely soluble (quickly converted into ammonia). Urea = NON protein nitrogen Ammonia utilized is dependent on how much energy is available in that particular diet.


As TDN (energy) increases so does the amount of microbial protein produced.

SYNCHRONIZE PATTERNS OF NH3 AND ENERGY SUPPLY Molasses: too fast – very fast energy release

Straw: too slow – highly undigestible

Cereal starch acceptable

CEREAL STARCH: IS ACCEPTABLE

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This graph shows when the energy will be released for a particular feed ingredient. Molasses fermentated quickly – quick energy release (slightly wasteful). Cereal fermentation is roughly the same as the NH3 energy release. Straw is undigestible – fermented slowly & thus energy releases slowly.

5. OTHER NUTRIENTS? sulphur S : N = 1 : (10 - 12)

for de novo synthesis of S A.A.

6. RUMEN DILUTION RATE rate of flow of digesta out of rumen (Units: % / hour)

slow residence time of bacteria in rumen maintenance energy energy for

growth

DILUTION RATE (% / h)

dil. rate maintenance expense energy for bacteria growth of bacteria

bacterial protein available to host

YIELD

MAINTENANCE

5

10

20

15

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MAX (THEORETICAL)

ENERGY EFFICIENCY OF BACTERIA GROWTH (bacteria mass/ATP)

2 4 6 8 100


When dilution rate is low (close to 0) most of the energy goes towards maintaining the microbes. From 2-8 % less energy goes into maintenance of microbes and more goes into the yield. 8% - approx. 80% of the energy goes into producing more organisms and 20% goes into maintaining the microbes that are there. Forage based diet – about 4%


Out of the rumen, into the abomasum, then into the small and large intestine. 8% is a high rumen dilution rate – meaning 8% of rumen capacity turns over and leaves every hour – this means that it takes approximately 12 hours to empty the rumen. 2-3% is a very low rumen dilution rate. The longer the microbes are sitting in the rumen the longer they have to be maintained – better off getting it out of the system ASAP to avoid “paying” for the maintenance costs. Slow rumen digestion rate = less removal of microbes = more energy needed to maintain the microorganism = less energy leftover for livestock growth.


In western Canada we have too much sulfur in our feed – because of high sulfur concentration in the water. Just be aware that there is a requirement for sulfur. We are basically concerned about reducing the amount of sulfur animals are eating.

Review again : Modern protein classification for ruminants is based on:

1. Solubility in rumen:

Totally and fast degraded to NH3

True protein and NPN

Determined in buffer in lab

2. Undigestible N (bound protein):

ADF-bound; perform N assay on ADF

3. Degradability in rumen:

Protein to varying degree is broken down to NH3.

The rate of breakdown depends on physical characteristics of the protein, and on

physical conditions in the rumen (dilution rate).

Measured by protein disappearance from porous nylon bags hung in the rumen of

fistulated ruminants.

4. Bypass protein (escape/undegradable):

The protein is not broken down in the rumen and arrives in the abomasum intact.

Measured by nylon bag technique.

Useful to target limiting amino acids to the S.I., and also to increase total protein

available to high producing ruminants.

Application in computer models – Cornell SystemProtein fractions in feed:

A NPN that is soluble and available in the rumen

B1 buffer soluble protein which is precipitated by tungstic acid. This fraction is

made up of soluble and degradable true protein which is degraded in the

rumen at a rate of 100-350% per hour.

B2 This is the buffer insoluble protein that is in the cell contents rather than in the

cell wall. It is degraded at an intermediate rate of 5 to 15% per hour.

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B3 This is slowly degradable cell wall protein that may be increased in heat

processed feeds. The rate of degradation of this fraction is less than 1% per

hour.

C This is cell wall protein and N which is not fermented by rumen bacteria and is

not available post-ruminally. It consist of N mainly associated with lignin,

tannins and Maillard reaction products.

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NPN – 100 g would be gone in 30 minutes (over 200%/hr) B1. highly soluble protein (120-250%/hr) – fermented so quickly they are converted to ammonia. B2. Insoluble (5-15%/hr) some will be broken down some wont – some will by pass. Slow degradation/conversion to ammonia. This means some of the protein will not be broken down into ammonia and will move into abomasum intact. C. not degraded/digested – bypasses right into the abomasum Graph 2: rapidly fermentable sugars – fermented very quickly – may cause the build up of organic acid & quick drop in rumen pH. B1. More gradual appearance of the energy from the carbohydrate (5-40%) B2. Fermentable cell wall – digested slowly (5-10%/hr). C. Unavailable cell wall – not digested at all bypasses the rumen fermentation system.

Factors affecting protein degradability Solubility in the rumen

Retention time in the rumen

Tertiary structure on the protein

Feed processing and storage (heat damage etc.)

Treatments to increase escape potential Heat treatment of the feed

Formaldehyde treatment

Tannin treatment

Encapsulation in a rumen inert polymer

PROTEIN REQUIREMENT

grams of cp / day = crude

should be in grams of digestable aa / day = lack data!

a large turnover of protein / day:

protein intake represents only 1/3 of total protein synthesis.

INTAKE 100 g / day

GUT SECRETION 70 g / day

=170 g

-10 g fecal loss

160 g absorbed

TURNOVER 300 g synth daily

100 g intake

200 re-used AA

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Mix with oil – oil covers the protein – the protein bypasses.


No longer used!


Causes some denaturing of the protein – different folding may make it harder to access by the microbes. Overdoing heat damage may make it indigestible to the cow itself.


3D structure – is it easily acceptable to the proteases in the rumen (synthesized by the microbes) or is it difficult to attack (less digestion).


The longer a protein sits in the rumen – the longer microbes have to digest the feed.


How quickly a feed protein is converted to ammonia.

PROTEIN – ENERGY INTERACTIONS

Deficiency of energy with normal protein intake: limits use of protein – AA converted to

meet energy requirement; stunts growth, reduced muscle mass but lean animal

Amino acid imbalance with adequate energy intake limits use of protein / amino acids for

muscle protein synthesis Deamination and use of aa for energy not used for protein,

but for fat tissue synthesis.

Outcome: growth with reduced muscle mass and increased fat deposition

% CPCP LIMITS GROWTH

CP ENERGYE LIMITS GROWTH

METABOLIC LIMIT

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GROWTH


Here is an animal – on y axis (growth of the animal), x-axis (increasing levels of CP in the diet), This is the ideal growth curve for any animal. If you have a energy limitation in the feed then growth will plateau – no energy to support muscle protein synthesis. Crude protein converted to energy (goes into adipose tissue). Here energy is limiting growth! Some energy will go back into growth (Very slow though) – stunted growth of the animal. Low protein intake – limits the growth potential.

B. Protein or aa deficiency

No particular signs: poor growth and poor performance

More extreme: anemia, low blood protein, edema, reproduction

KWASHIORKOR = PROTEIN in MAN

MARASMUS = ENERGY in MAN

PROTEIN REQUIREMENT

Requirement: minimum amount of a nutrient needed for a specific function

Allowance: amount provided in diet to satisfy requirement + may contain a safety

margin

REQUIREMENT

EMPIRICAL THEORETICAL

(TESTS) FACTORIAL OR

PARTITION APPROACH

LITERATURE VALUES OFTEN A COMBINATION of both

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Safety margin


Energy deficiency in people


Protein deficiency in people

MINERALS

INTRODUCTION:

26/90 elements are essential (required to maintain life)

Major or macro (measured in %): S, Ca, P, K, Na, Cl, Mg, Fe

Minor or trace (measured in mg/kg, ppm or ppb): I2, Cu, Zn, Mn, Co, Ni, Mo, Se, Cr, F, Sn, Si, V, As

Modern definition of essential: Consistently impaired function when deficient Supplementation of the mineral prevents or cures symptoms >1 Investigator >1 Species

Major advances in mineral nutrition research as a result of new analytical equipment. Atomic absorption spectrophotometer is the work horse.

New experimental conditions: ultraclean lab equipment and animal housing filtered air synthetic diets

1969: ration with 5 ppb Se showed Se deficiency

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Is arsenic really an essential mineral? Its also known as a poison. Brings home the point that many minerals can be toxic, but also essential. Depends on the DOSAGE.


Deficiencies are usually localized to a certain geographical area. Incidence of problems are high due to minerals.

Fig. Dependence of biological function on tissue concentration or intake of a nutrient

Each element has its own specific curve Different tissues or enzymes will also have different curves i.e. some enzymes in

different tissues have different sensitivities depending on essential nature of enzyme function

For each element there is a range of safe and adequate exposures in which homeostasis is maintained

Every element is potentially toxic In practice marginal areas difficult to define (sub-clinical) leading to marginally

reduced animal performance on a large scale ------ high $ impact Clinical deficiency is only tip of the iceberg and easily corrected

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Rely on ration formulation, feed analysis to help deal with the subclinical symptoms. Also look at what mineral deficiencies/toxicities are common in a certain area. Eg. In western Manitoba copper deficiency is a common problem with cattle. Eg. In fraser valley, BC – there are entirely different soils than in Kelowna, etc. Eg. Areas with mining – is the soil polluted, air polluted – can impact mineral toxicitiy/deficiency.


X axis = increasing levels of minerals. In the graph you get a flat bell curve. You get a flat plateau over a range of mineral concentration. When minerals are limiting – function is decreased/low. Then as you supplement the mineral their function increases until it reaches plateau. When you keep adding more they become toxic and function decreases and may lead to death. Homeostasis of Mineral Metabolism: Optimal function is in the plateau – we know that this is the result because animal can adapt to varying mineral concentration through homeostasis. On the low end of the plateau – animal can adapt to low mineral concentrations while maintaining optimal function. When you start to move into the subclinical zone in both toxic/deficient region – you get subclinical deficiencies or subclinical toxicity Subclinical – means no obvious symptoms – nothing will trigger you to think there is a mineral deficiency. Clinical – means there are obvious symptoms – can help you to diagnose a mineral deficiency/toxicity. In Animal Agriculture: MOST of the cases we see are dealing with SUBclinical deficiency/toxicity. If you go into a herd and you see a few animals with clinical symptoms, then the other animals are likely in the subclinical zone.


Showed that selenium is actually an essential mineral, even though it is also toxic.

Single element can influence several metabolic processes.

Example Cu

1. Cytochrome oxidase involved in ATP trapping- affects all energy dependent processes- affects a wide range of processes- differences between tissues in terms of effects and priority

Lesion: nervous tissue specific effectLesion elsewhere non-specific

2. Tyrosinase converts tyrosine to melanin (pigmentation) & requires Cu as a catalyst.

Cu deficiency: First sign = depigmentation

3. Lysyl oxidase connective tissue synthesisTropoelastin elastinCu deficiency connective tissue disorders, and cardiovascular disorders

Functions fail at different times and therefore symptoms may indicate severity of deficiency or toxicity

Separate graphs: Depletion phase in terms of pools and elements

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Specifically, in the arterial wall – problematic in the cardiac arteries. CT becomes weaker – may get a spontaneous rupture of artery wall which results in instant death. Species most at risk is poultry. Syndrome – falling death disease (walking around and all of a sudden they collapse – due to arterial weakness – results in a massive bleed out – basically have a heart attack then drop dead)


In black cows – copper deficiency will appear as some of their hair will be depigmented or will manifest as a reddish/copper colour – or there will be a change in pigmentation (lack of it). Cattle are most prone to copper deficiency.


If reduced in nervous tissue – you get paralysis in animals. In lambs – Cu is very specific in nervous tissue & leads to hind limb paralysis. This happens in sheep but not in chickens – species differences.


He will talk about copper deficiencies in western Canada, specifically the prairies (low Cu in soil – plants grown here will be low in Cu as well).

Length of depletion phase can be variable depending on complicating factors such as chelators (molybdenum and sulfur), stress, disease, genetics

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Pools = storage sites for minerals. Copper is stored in the liver, plasma, and in the tissues. Trace minerals are stored within the body – the most important organ for storage of trace minerals is the LIVER. It is our reserve for trace minerals (not macro minerals which are stored in skeleton) What you see here: The liver is the reserve & had a storage of copper – it is depleted at a rapid rate when they are fed a 0% copper diet. Plasma copper levels are maintained at a normal range by mobilizing the reserves stored in the liver. When the liver is very depleted (20%) left – then you start to see a decline in plasma copper as well. Tissue copper starts to decline as well until you reach a level where clinical signs manifest. NEED to be aware that this is happening: can’t tell whether or not the animal is relying on the liver or their feed. When you take a blood sample – plasma copper levels may come back as normal – things may not be fine – YOU do not know that the animal is depleting copper from their liver. It is misleading (false +ve) This whole depletion curve can take about 2 months. If you sample later into the deficiency and send a blood sample off then it can come back as OH – yes the animal is copper deficiency (true –ve) Blood Analysis – not the best way to figure out if there is copper deficiency. More reliable indicator is to measure liver copper (do a liver biopsy – NOT liked by farmers – risk association, lots of work, infection risk). Is not practical. What do you do then?? A feed analysis – a simple b& reliable method

Depletion rate is a function of: Reserve pool Rate of mobilization Requirement

Length depletion phase can be variable depending on complicating factors

Homeostatic control: WHY???

Large variation of levels of minerals in feeds; even within plant species

Factors responsible:

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Minerals are very different in their behaviour. When you deplete the different minerals: Zn has a very rapid rate of depletion Cu & Se have a slower rate of depletion. Zn may be depleted from its reserve so quickly because: animal uses is very quickly, or their reserve pool is smaller.

Genus, species or strain of plant Type of soil Rate of plant growth Climatic or seasonal conditions Irrigation Stage of maturity Soil management (fertilizer, pH) Herbicides Environmental (acid rain, smelters, traffic pollution) Harvesting of plants (leave loss; soil contamination, equipment

contamination)

50 fold differences in concentration10 fold differences in concentration within species

Degree and method of homeostasis vary

Rejection of excess is as important as absorption and retention:Earth’s crust Mn 15X in conc than ZnForages Mn about same conc as ZnBody Mn about 1% of Zn conc

Homeostatic control routes:1. % absorbed2. Excretion via urine3. Tissue deposition in harmless and /or mobilizable forms4. Secretion into milk5. Endogenous excretion via feces (bile)

Minor routes: exhalation, sloughing of cells skin, hair, wool, perspiration

Mineral requirement:

Affected by: Type, composition of product (physiological function) Type of animal, species, breed, sex, age Level and chemical form in diet Amount and nature of feed consumed

Acidic; basic; chelating agents such as phytate, oxalates Non-dietary environment Stress affects homeostatic ability

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May be able to meet its mineral requirement under ideal conditions. When environment changes there may be a mineral fluctuation.


Lots of chelators in plant material – these tie up Ca/P & can lead to major deficiencies.


If its more acidic – then calcium is more available (bc it more soluble at a low pH – whereas Phosphorus is not).


Exotic beef cattle have a higher copper requirement compared to aberdine angus or Hereford cattle. Also black faced sheep (saffolk) has a greater tendency to be more sensitive to copper toxicity.


Lactation/Egg laying require an enormous amount of calcium.


Can do a mineral composition analysis on hair – is an examples of LONG TERM mineral status in an animal.


Iodine/selenium can be volatile.


Enterohepatic circulation – minerals secreted in the bile, minerals can be reabsorbed from the bile or lost in the feces.


Can measure trace mineral composition in milk & relate it back to the nutritional status of the animal.


Trace minerals are stored in the liver – excess intake will cause build up into the reserve. Ca/P/Mg – primary reserve is in the bone.


Another way to get rid of excess minerals – tightly controlled. One of the most common ways to rid of minerals.


Can have a range from about 10-89% - which is actively controlled. Is a function of passive diffusion across GI wall & active transport (regulates whether a mineral is absorbed or rejected).


Lead paint on farming equiptment and used to paint barns.


Traffic beside pastures makes lead go into the plants that are eaten by cows. Dairy cows that eat in pastures near the roads have higher levels of lead in their milk. In UK – their soil is contaminated with molybdenum – a consequence of environmental pollution.


Cereals, barley, wheat, corn – has a Ca level of about 0.2% calcium. Alfalfa – 1.2 % calcium In grasses 0.8-1% calcium Stem vs leaf – young vs old ( has an effect on the mineral content. Monoculture – only grow one type of plant in a field – results in higher risk – animal has to rely on 1 plant species to provide all the minerals. A pasture with a range of species of plants – animals grazing here will likely get a better range of minerals from them. Horses grazing in pastures in southern Saskatchewan with a high incidence of stink weed – has a high concentration of glucosinolates which are basically interfering with iodine metabolism and thyroid function. Trying to link hypothyroidism in foals to mares eating stinkweed. Diversity of plants in the field can be positive or negative as well.

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Don’t memorize. Shows the complexity of all the interactions that occur between minerals. We feed minerals to the requirement – very high Ca levels interfere with P, Mg, Zn absorption. Zn can be so high that copper cannot compete with Zn. Sulfur interacts with selenium – when you have high sulfur intake (happens a lot in prairies from the water) can cause a low selenium absorption – and may lead to Se deficiency.

Calcium and Phosphorus nutrition:

inter-related both need to be in adequate amounts Ca:P ratio important dependence on vitamin D

Bone: 25% ash (fresh)45% water10% fat20% protein

Bone (dry-matter basis and fat-free basis): Ash 55% Protein 45% Ca:P = 2:1 Also contains Mg, Na, Sn, Pb, F, S, carbonate and citrate

Bone types:1. Soft: readily mobilized, amorphous2. Long: harder, static, crystalline

Bone is characterized by active metabolism and constant turn-over. Ca and P exchange occurs across bone – blood barrier.

Deposition of salts depends on: concentrations of Ca and P solubility constant Ksp hormonal effects (calcitonin and PTH) weight stress leads to remodeling and strengthening

Abnormal bone conditions:

RicketsOccurs in growing animals only inadequate calcification of growing bone occurs with low concentrations of Ca or P in feed occurs with low absorption efficiency of Ca or P Vitamin D deficiency or phytate or abnormal Ca:P ratio

Symptoms of rickets: reduced ash content of bones rubbery bones and beaks enlarged joints bending of ribs bent legs, arched backs, lameness, bone fracture

Rickets can be corrected by supplementing Ca, P and vitamin D in early stage.

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More collagen there.


Inadequate Ca, P, or Vit D! Incidence rate in farm animals is VERY rare – in humans not rare.


Demineralization than remineralization. If you put too much pressure = fractures.


Deposited into hydroxyapatite crystals in the bone.


Pelvis, ribs, sternum, shoulder blade – readily turnover – crystal structure easy to mobilize Ca/P from. If an animal goes into Ca deficiency – soft bones will be mobilized to provide the Ca.


Ash= minerals Bone meal is a good source of Ca/P – also a good source for protein/energy.


Cannot consider calcium without considering phosphorus – ratio needs to be 2:1. Also have to consider Vit D – as a hormone is essential for Ca/P from the gut.

Osteomalaciaas rickets, but occurs in mature animals sub-normal intake of Ca and P or reduced absorption high parathyroid hormone concentration in blood bone demineralization associated with pregnancy or lactation bone fracture (pelvic at calving) higher incidence in dairy cows and laying hens

Osteoporosis reduced absolute amount of bone, but with normal composition high incidence in middle-aged females: long term sub-normal Ca intake increased bone resorption estrogen provides “protective” effect

Nutritional secondary parahyperthyroidism (PTH) AKA big head disease in horses low Ca and high P in diet >> Ca deficiency and interference of Ca absorption by high P

content low blood Ca >>> high PTH>>> bone mobilization >>> normal to low normal Ca, but

very high P in blood connective tissue invades demineralized bone resulting in deformity occurs when horses are fed grain rations without supplements

Function in soft tissues:

Ca: Blood clotting (thrombin) Enzyme function: lipase, ATPase Nerve function: nerve/muscle action potential Insulin release beta-cells pancreas

P: Energy metabolism Acid-base balance

Deficiency (not enough):

Ca: Tetany (milk fever in dairy cows) Increased blood clotting time Reduced insulin release (could lead to ketosis) Skeletal

P: Reduced fertility!!!!!!!!!!!!!!! Reduced feed intake, pica

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Strange appetite – start eating weird things. Eat less – don’t get enough energy & results in weight loss.


Milk Fever – when a cow after calving goes down w/ tetany/paralysis – can’t get up. Infuse Ca subcutaneously to revert the situation. Cow goes through calving process which is stressful which reduces GI function for a few days (reduced absorption and reduced eating). Immediately around calving get induction of milk synthesis in the mammary gland (uses up a lot of calcium) – Calcium requirement switches from being very low – to very high in a matter of a few hours. How does the cow compensate? – not absorption, cant mobilize bone immediately (12-24 hrs). Cow cannot adust to an extremely rapid change in calcium requirement. Prevention: feed the cow a low calcium diet before calving so they are physiologically tuned to be very efficient in Ca absorption/metabolism. At calving we switch cow to a high Ca diet – w/ increased efficiency – the cow can absorb Ca more readily.


Calcium deficiency can interfere with pancreases ability to secrete insulin when blood glc levels are high. Can make diabetes worse.


Such a gross deficiency in calcium that animals secrete a gross amount of PTH (stays elevated). High PTH causes bone demineralization (tries to increase blood calcium level) – especially when you cant absorb it in the gut (when not being fed the correct amount). Effects the skull – demineralization & invasion of connective tissue – changes skull symmetry. Causes a skull enlargement. Encountered often in acreage owners that think horses should eat just oats (low in calcium!).


Starts at puberty – is a lifetime of low-calcium – then manifests after women hit menopause. Beverages high in phosphoric acid – phosphorus increases and calcium doesn’t – messes up the Ca:P ratio.


Increases osteoclast activity – more absorption but also mobilizing Ca from the bone at the same time. Gradual weakening of bone over time. During periods of extreme stress on bone or high Ca requirement can lead to bone fracture (eg. Pelvic fracture during birthing process).

Skeletal

Toxicities (too much):

Ca: Excess mineralization (osteopetrosis)

- in soft and vascular tissues- arthritis (ie high Ca diet breeding bulls results in poor breeding performance)

P: Laxative Bone resorption (big head) Kidney stones

Ca and P Absorption: site and pH

Ca: duodenum, pH 6.5 favours increased Ca absorption

P: ileum, pH 7-7.5 favours increased P absorption

Diet acidity: Increased acidity of diet favours increased Ca absorption (dairy cows to prevent milk

fever)

Ca:P ratio: High Ca in diet CaP salt precipitation in ileum High P diet CaP salt precipitation in duodenum

Chemical form of Ca and P and availability: Inorganic form is better available Organic form is often chelated and poorly available

Common chelating agents:

Phytate: chelates P, Ca and various trace metals and amino acids

50-80% of P in grain is in the phytate form and only 0-30% available to monogastric animals

Phytate also widely present in other plant sources

Rumen microbes produce phytase, and this phytate P is fully available to ruminants.

Use of feed biotechnology to reduce phytate impact:

1. Produce phytase enzyme and supplement to diets for pigs and poultry.

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Addition extremely common in swine and poultry diets – one day it may be added to dog foods. It makes phosphorus more available to the monogastric animals.


Alfalfa hay is very high in calcium – they get crystal buildup in the joints of the legs and they become arthritic/sore & they will not breed.

2. Produce transgenic grains and canola incorporating a microbial phytase gene.

- Increases availability of phytate P- Reduces the need for P supplementation in rations– Overall less P excretion in manure and less impact on environment

Oxalic acid:

- Chelates a wide range of minerals, but especially Ca- Oxalic acid + Ca Ca oxalate precipitates- Can lead to formation of calculi (kidney stones)- Oxalate commonly high in beet tops, rhubarb, spinach, swiss chard, chocolate- Oxalate can be high in forages- Reported instances of oxalate-induced abnormal skeletal development in foals, where

oxalates bound the equivalent of 0.8 % of dietary Ca.

Ration ingredients:High fat diets formation of Ca soaps

Diet mineral interactions: Fe, Al, Hg, Be, Sn can all interfere with P absorption

Note:Ca and P absorption is critically dependent on vitamin D

Magnesium

Function: Component of bones and teeth Catalyst of many enzymes, including cholinesterase (nerve transmission) and

ATPase (energy metabolism) Component of chlorophyll in plants

Location of Mg in body:- 60% in skeleton- 40% throughout (Intracellular fluid – highest [ ] after potassium)- Second highest cation concentration in intracellular fluid

Absorption of Mg: Both diffusion and active transport Slower than that of Ca Affected by:

- NH4+

- K+

- Na, Ca, P, SO4, phytate, oxalate

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Reflective of the amount of protein in the feed.


Absorption in the gut – but absorption into the plant from the soil is similar!. NH4 interfers with uptake of Mg in the gut and into the plant. Deficiency of Mg is prevalent in ruminant animals, especially ones that graze.


For the breakdown of acetylcholine.

High K+ (over 2%)

1. High DCAB (450 vs 250 meq/kg) causes alkalosis reduced Ca and Mg absorption milk fever and grass tetany

2. In ruminant Mg mainly absorbed through rumen wall - active through Na-linked carrier. High K+ reduces transmembrane potential of epithelial cells and thus Mg absorption.

Mg deficiency: Hypomagnesemia Anorexia Grass tetany – grass staggers – hypomagnesemic tetany

(reduced cholinesterase activity) Vasodilation Malformation teeth

Requirement:- 0.3 % of Dry Matter- Use Mg sulfate or Mg oxide to supplement

o Can infuse animal via IV fluid or by sprinkling it on their pasture.

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Most common in dairy cattle – where there are high quality lush pastures.


Dietary cation- anion balance.

Na, K, Cl:

Required for: Osmotic pressure Acid-base balance Nervous function Nutrient transport Water metabolism Enzyme function HCl production stomach

Na deficiency:- Pica (depraved appetite), reduced appetite, reduced growth.- Na is low in plants and Na supplementation (as NaCl) of animals is always

required- Feed NaCl (white salt): increase appetite and palatability

o Red Salt – NaCl + iodineo Blue Salt – NaCl + iodine + cobalt

K deficiency:- K is high in forages and low in grains and concentrates.- Normally K intake is adequate, when a substantial amount of forage is fed. - Dairy cattle with high milk yield (high K loss in milk) and that are fed more grain

and less forage to meet the energy requirement for milk production can become deficient in K.

- Requirement is 0.8 %

There is some evidence to suggest that feeding of a high K diet (1.5%) during a limited period may be beneficial when animals are stressed and have reduced feed intake. Heat stress Shipping stress Ration change Lactation

Electrolyte balance in feed:- anion-cation balance- alkaline alkalinity - affects acid-base balance, performance, and utilization of amino acids- measured as (Na+ + K+ - Cl-) ~ 25 milliequivalents / 100 g feed (250 mEq/kg)- optimal growth around 25 milliequivalents, as less energy is expended on acid-

base balance and thus more is available for growth (see graph)

Sulfur:

- Required especially for ruminants to allow S de novo amino acid synthesis in rumen.

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Makes methionine and cysteine. As well as some B vitamins.


Can influence the acid-base balance of the animal.


If you feed dairy cattle more grain/concentrate and less forages – you are lowering the potassium intake of the animal. Not good because lots of potassium is incorporated into their milk.


Cobalt is an essential mineral for production of Vitamin B12 in the rumen fermentation system.


Used on a farm to feed monogastrics – iodine is usually deficient not much in plant material (except on coastal regions where there is usually enough iodine in the plants).


When there is reduce appetite – automatically should be thinking there is some kind of mineral deficiency.

- Recommended S : N = 1 : (10-12)- Also, required for thiamine and biotin vitamins- In Western Canada, we are mostly concerned about high S intakes.

High S in ruminants - with Mo, formation of thiomolybdate and decoppering effect; CuS.- sulphate and thiosulfate inhibit the uptake of selenium - retention of both calcium and phosphorus is reduced by the addition of sulphate

to diets - interference with ruminal thiamine synthesis, resulting in primary thiamine

deficiency or secondary thiamine deficiency (thiamine anti-metabolite formed in rumen).-In both cases abnormal glucose metabolism in brain cerebro-cortical

necrosis, also known as polioencephalomalacia (PEM)

- Clinical Features of S Induced PEM: -Signs appear between the 3rd and 8th week of exposure -Initially affected animals exhibit transient attacks of mild excitation, loss of

appetite and restlessness-some affected animals may recover spontaneously -growth of these individuals is stunted

- Progression of clinical signs reflects development of necrotic lesions in the cerebral cortex of the brain. -aimless wandering-head pressing -hyperexcitability -rigidity -opisthotonos

- In severely affected animals the signs reflect severe necrotic lesions in the cerebral cortex -recumbency -violent convulsions-coma and death

- Pathological Features of S Induced PEM-Extensive necrotic lesions in the cerebral cortex -Polioencephalomalcia (softening of the gray matter of the brain)-Cerebrocortical necrosis

- Note that a diet with high content of simple carbohydrates can also induce PEM

(through thiamine anti-metabolite formed in rumen).

Iron:Fe present in small amounts (4-5 g in humans):

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Baby pigs are very prone to iron deficiency, usually because of management.


In Cuba, they fed cattle a lot of simple sugars that are rapidly fermented into organic acid that resulted in the formation of the thiamin anti-metabolite! How to correct it? Add thiamine to the feed or give the animal an injection. Do not feed so much simple sugars and make sure there is not too much sulfur in the feed.


Primary – Not enough thiamin is being synthesized. Secondary - Formation of abnormal thiamine – gets absorbed and enters metabolic pathways – it binds but is NOT biologically active.


Vice versa also occurs – when selenium is high the uptake of sulfur decreases. It also replaces disulfide bonds with diselenium bonds – makes enzymes non-functional, protein synthesis and keratin formation are all damaged/impaired. If animal has a selenium deficiency the treatment is to give more sulfur to counteract the effects.


Family of compounds – is one of the strongest known chelators of copper. In rumen environment, they bind copper and make it unavailable for absorption. It is also absorbed into blood circulation and travels to the liver and chelates the copper out of the liver reserves! Can use thiomolybdate as a treatment in people that have Wilson’s disease (copper toxicity).


More and more molybdenum as you move from Saskatchewan to Manitoba.


Primarily coming out of their drinking water – well water, etc.

- 70% is in hemoglobin & myoglobin (gives meat red colour)- gut mucosal cells, liver, spleen and marrow are storage sites- present in plasma as transferrin- component of oxidation-reduction enzymesStorage of Fe in proteins:1. Ferritin = protein with 20% Fe content and soluble2. Hemosiderin = protein with 35% Fe content and insoluble

Fe absorption:

Active absorption:First step in lumen: Fe3+ Fe2+

Diet Fe3+ (ferric) must be reduced to Fe2+ (ferrous) before it can be absorbed into mucosal cells.

Vitamin C is a useful reducing agent.

Note that ferrous iron is again oxidized to ferric iron in the mucosal cell. The enzyme ceruloplasmin is an important oxidation enzyme for this reaction.

Ceruloplasmin requires Cu for enzymatic activity, and this explains why anemia can be symptom of Cu deficiency.

Efficiency of Fe absorption:

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Ceruloplasmin is an enzyme that requires copper as a catalyst – thus copper deficiency can cause secondary anemia . This enzyme converts Fe2 to Fe3 which is moved into blood (controlled by protein trasporter saturation) and binds to transferrin and then moved into tissue as ferritin.


Ferritin is soluble (meaning its very available for use) Hemosiderin is insoluble – helps animal to deal with excess iron & helps with iron toxicity.

- Fe status of animal and feedback inhibition at gut level- Low pH increased absorption- Vitamin C- Chelating agents:

- his, lys increase absorption- lactoferrin in human milk is positive- phytates can reduce Fe absorption

- High P, Zn, Mn, Cu, Cd can reduce absorption

Range of homeostasis: 5-60% absorption efficiencyNormal: 20 % (on which requirement is based)

Fe deficiency:- Anemia - microcytic (reduced cell size) - hypochromic (reduced hemoglobin)

Symptoms of Fe deficiency:- Reduced activity (lethargy)- Palor (paleness)- Shortness of breath

Among farm animals baby pigs are most susceptible to Fe deficiency.

Baby pigs:

1. Low body reserves at birth2. High growth rate (1 to 18 kg in 6 weeks) high Fe requirement for increased

blood volume.3. Sow’s milk contains little Fe.4. Low feed intake.

Inject 100-200 mg iron dextran at birth.

Rooting behaviour of piglets on dirt floor or in the wild would allow adequate iron intake.Farmers used to throw grass sod in pen for this purpose.

White veal production (Europe):- Feed calves milk replacer with low Fe low myoglobin in muscle.- Major animal welfare concerns. Practiced mainly in France and Italy, with some

in Quebec for French market.

Iodine:

Component of thyroid hormones T3 and T4

Three forms of thyroid iodine deficiency:

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Uptake of iodide is competed with by thiocyanate which decreases the amount of iodide that is uptake. Iodide attached to tyrosine rings.


These animals are purposefully made iron deficient – which means less myoglobin forms and meat appears white! Iron deficiency makes these animals prone to infectious diseases and thus they need to be fed lots of antibiotics. Animals put into crates – so they don’t move – so energy used for growth instead of movement. There are now standards in place for white veal production.


Baby pig increases 18-fold in 6 weeks – their blood volume also increases a lot – and this drives up their iron requirement – Normal procedure is to inject the baby pig with iron at birth. How do they then survive in nature? Rooting behaviour in soil allows adequate iron intake.


Usually not a concern in farm animals – most feed supplies are contaminated w/ soil which contains iron.


Wide range of efficiency – nutrient requirement tables are based on an absorption efficiency of 20 %. Low pH causes increases solubility and absorption of iron. Vitamin C also causes increased absorption of iron. Chelating agents: histidine/lysine chelates iron and increases absorption because they are being absorbed through AA absorption pathway rather than the iron absorption pathway. Phytates – reduces iron absorption. Metal compounds can reduce absorption.

1. Simple primary deficiency (not enough iodine in soil or feeds)2. Competitive inhibition of iodide uptake in thyroid gland (i.e. by thiocyanate)3. Non-competitive inhibition through reduced organification of iodide into thyroid

hormone (i.e. goitrin, oxazolidinethione (OZT))

1. Iodine content in feeds is low throughout the world except in coastal areas. Therefore, to prevent primary deficiency iodine must always be supplemented to animals and humans (iodized salt – red salt for animal supplements).

2. Presence of goitrogens is variable and feedstuff dependent.Glucosinolates are a class of goitrogens that release thiocyanates (competitive inhibition).Goitrin is a non-competitive class of goitrogens

3. Rapeseed is high in glucosinolates and therefore the meal was not very suitable for animal feeding.

- Canola is a much improved low glucosinolate rapeseed variety, and is very suitable for feeding.

4. Goitrogens are found in a wide range of plants (natural pesticide), including the cruciferae family with cabbage, cauliflower, brussels sprouts, mustard, horse radish, broccoli. soybean

Iodine deficiency signs:- Goiter - Low BMR, increased fat- Reduced fertility- High mortality at birth (fetus with goiter)- Myxedema (pooling of plasma)- Alopecia (hair loss)

Iodine requirement (normal conditions):- 0.2 to 0.3 ppm- 0.5 ppm for dairy cattle (iodine is secreted into milk at a high rate)- The feeding rate must be increased (2-3 times) when goitrogens are present in

order to compensate for competition.

Iodine supplements:

Salts: KI, KIO3

Ethylenediaminedihydroiodide (EDDI; “organic” iodine) is also available. It is used for the prevention of foot rot, but this application is of questionable value.

The dosage of EDDI as iodine is very high and raises concern about iodine toxicity in animals and humans.

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More iodine in the feed means more iodine in the milk.


Under IDEAL conditions – but due to goitrogens in the plants used in animal feed you still must over feed iodine because of competition.


In 1920s – no iodized salt – so goiter was prevalent. Also present now a-days in Bolivia.


There is about a hundred different goitrogens – some are found to have a health benefit – enhance cell turn over & lowers incidence of colon cancer in people.


Is used as a protein supplement – but not suitable for feeding because of the high glucosinolates which reduce iodide uptake.


Are a class of chemical problems that cause goiter (enlargement of thyroid in response to iodine deficiency) which is an adaptive response to the gland trying to trap more iodine. Found in many different feed types – glucosinolates release thiocyanates which compete for iodide transporter.


Anywhere in the world that is not on the coast is usually deficient in iodine. Salt is iodized to prevent iodine deficiency in humans. In Britain they do not have iodized salt – they estimate that ½ of british population is sitting below the recommended level of iodine & thus thyroid problems are quite prevalent.

Normal intake of a dairy cow is between 5 and 15 mg/d and milk iodine normal range is 50-300 g/L.

EDDI feeding results in intake of 200 mg/d and milk iodine levels up to 2000 g/L.

Human iodine requirement:Children 50 g/dAdults 120 g/d – 150 g/d

High iodine-milk consumption results in iodine intakes in children (0.5-1L/d) is more than 10x requirement toxicity concerns based on milk intake alone. Also consider iodized table salt, and salt in condiments, chips etc.

Dairy farm families are at greater risk than the regular consumer, because they do not have the benefit of the pooling effect (mixing of high with low iodine milk) in case the on-farm milk is high in iodine.

Iodine toxicity symptoms:

- Increased salivation and lacrimation (symptoms are similar to those from IBR (infectious bovine rhinitis)).

- Reduced fertility- Reduced productivity- Immuno-suppression

Manganese Mn:

Required for:- Enzyme function; oxidative phosphorylation, pyruvate carboxylase.- Chondroitin sulfate formation (cartilage)- Steroid synthesis from cholesterol

Deficiency signs:1. Leg-bone:- Newborn calves-lambs: weak or stillborn, with twisted or knuckled over pasterns -

contracted tendons- Lameness, short bowed legs- Perosis or slipped tendon in poultry (common symptom)

2. Reproduction:- delayed or silent estrus- reduced conception rates – embryonic death– reduced libido– reduced spermatogenesis

Requirement:

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If seen you can narrow down the deficiency to being either manganese or biotin!


In addition – we use a lot of iodine for sanitation of the dairy barns – which can end up in the milk. Iodized salt – troublesome now because humans now consume a lot of salt in their diets – now government has to lower the iodine levels in the salt or restrict the use of iodinized salt.


Enough to cause iodine toxicity in cattle & increases the iodine in milk greatly. Milk can only contain 500 ug/L to be fit for human consumption.

- Is higher for reproduction in general and in poultry.- Range of 20-40 ppm, and 55 ppm in poultry.- Supplement with MnSO4, MnCO3, MnO.

ZINCComponent of many enzymes including RNA and DNA polymerases, carbonic anhydrase, alkaline phosphatase, LDH

Absorption: Primary interference by divalent cations Cu, Ca, Mg Phytate interference

Deficiency: Reduced growth - anorexia Hyperkeratinization of epithelium: parakeratosis Infertility in males Impaired wound healing Liver produces IGF-1 – mitogenic – increases growth (bone, muscle,

mammory)

Requirement:40-50 ppm; ZnO, ZnS04

COBALTDiscovered by E. Underwood around 1935Most commonly deficient in ruminants:

1. Rumen microbes + cobalt vitamin B12 cyanocobalamine2. Required for propionate metabolism in TCA cycle: Impaired

gluconeogenesis

Deficiency results in WASTING DISEASE

Feed is available but animal starves to death

Requirement: 0.1 ppmCoO, CoS04, CoCI2, CoC03

Blue Salt: Co + Iodine + NaCIBulletsRange MixFertilizer

COPPERVery important in the prairiesOften deficient in cattle exposed to variable mineral intake:

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Range Mix – loose mineral mix with Ca, P, Fe, Co, etc. Animals can lick it up when they desire. Bullets – an iron metal object that is quite porous – it is impregnated with a bunch of trace minerals and put into the reticulum of the cow for slow release of minerals.


Animals have feed available but they are starving to death and are wasting away until they die. Had a massive impact on the sheep industry in Australia. Cobalt was the common factor for the animals that were effected by wasting disease – rumen microbes need cobalt to make Vit B12 – essential for driving propionic acid into gluconeogenesis – then the sheep could not produce glc from gluconeogenesis and leads to hypoglycemia. A lot of soils are deficient in cobalt – usually needs to be supplemented. Cobalt requirement is unique for ruminants because their microbes synthesize B vitamins from cobalt. Ruminant have a higher B12 requirement than monogastric animals because they are always doing gluconeogenesis compared to other animals that only do gluconeogenesis during a fasting state. Monogastrics get a supplemented Vit B12 – plant is not a good source of this – but meat products are good sources of it. In humans our Vit B12 intake is from fermentation products and animal product that we consume.


When you want high animal growth you need high IGF-1. GH from pituitary gland and nutrition (Zn) are what influences the amount of IGF-1. Nutrition is most important – Zn is an absolute requirement – when you have a Zn deficiency IGF-1 levels drop drastically. Dog frame/size – there is a direct correlation with IGF-1. If you measure plasma IGF-1 it is a very good indicator of animal health – better than serum albumin. Serum albumin levels are indicative of the protein status.


Rough hair coat – and lots of skin wrinkling in pigs. In cattle – poor hair coat, ulcerations, foot lesions DO NOT CONFUSE Zn with Vit A deificiency If there is an exam condition about skin condition, there are a few suspects: - Zn - Vit A


If there is a Zn deficiency there would be a problem with RNA and DNA polymerization, transcription, translation, mitosis, etc.

Breeding and pregnant most at risk

Copper Deficiency signs:1. Anaemia

a. Iron transport – ceruloplasminb. Indirect Fe deficiencyc. RBC synthesis

2. Achromotricia (depigmentation) Melanin synthesis tyrosinase - Cu dependent

3. Neonatal ataxia Swayback (Lambs) Reduced cytochrome oxidase

4. Falling Disease (Sudden Death)Bone deformities, reduced elastin and collagen synthesisLysyl oxidase is Cu dependent

5. Scouring or diarrhea6. Defective keratinization7. Hereford/Angus have lower copper requirement than the animals that

came from Europe like the charolais, symmental, etc.

ABSORPTION: Upper small intestine Plasma: RBC =1:1 80% of Cu in plasma in ceruloplasmin

Excretion:Increased with Mo, Sulfur, Cd, Zn

Cu Status Measurement:1. Feed analysis2. Liver Cu (invasive)3. Plasma ceruloplasmin4. Plasma Cu

Copper Deficiency in the Prairies:1. Simple Primary Deficiency:

Low Cu in Feeds < 5 mg/kg Depends on soil type, management, etc. Throughout western Canada

2. Secondary Deficiency: Most important cause of Cu deficiency Associated with high S and/or Mo intake

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Major chelators for copper.


Soils are low in copper in the prairies – so feedstuffs will be low in copper as well.


First thing you should do when deficient in trace minerals!


Can use either one. REMEMBER – these concentrations can look normal even though the animal is relying on the reserves in their liver.


In birdies.


Can lead to hind limb paralysis.

Cu and SULFATES: Source of S is ground water: Greater than 800 ppm is bad Mean sulphate in SK, AB, MB is 1800 ppm Deep wells always suspect Shallow wells less Surface water acceptable.

MOLYBDENUM: Mo levels in feeds depend on Mo in soil: focus on Eastern Sask. and

Manitoba (increases as you move from SK to MB – swan river, MB has Mo of 12 ppm)

With NORMAL S intake: 800 ppmCu: Mo = (2-3):1 Manageable - SK Cu: Mo = 1:1 Difficult – MB

With HIGH S intake:The combination of Mo and S is problematic Formation of thiomolybdates (TM) under reducing conditions in the rumen:

1. TM chelation of Cu prevents absorption2. Thiomolybdates decopper animal

Recommendations: Cu requirement is 5-10 mg/kg For most of the prairies with moderate S (1800 ppm) and moderate Mo (1-2

ppm): 25 mg Cu/kg DM – 25 ppm Pregnant animals up to 55 ppm

With elevated Mo and Moderate S: Undefined but probably 55 ppm

Use of Cu injectables? Decoppering effect?

SUPPLEMENTATION:Salts: copper sulfate Trace mineral mixes: force feed, free choice, salt blocksInjectables: Cu glycinate; Cu calcium EDTAOther: Drinking water supplement, wires, degradable glass

COPPER TOXICITY: Sheep are very sensitive to Cu:

Common cattle grain feed supplements with 25 ppm Cu KILL sheep!

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Almost unmanageable situation because as you supplement the copper I diet it would just be chelated. Injectables bypass the rumen fermentation system, you can also implant copper wires under the skin. Might not help because of the decoppering effect of Thiomolybdates.


CANNOT give this amount to sheep – people think you can give this to them because they are also ruminants but they are extremely susceptible to copper toxicity when fed a diet with 25 ppm of copper. Instead they should be fed a diet with 5 ppm.


More Cu lost in feces and TMs also chelate the copper in the liver and reduces/removes the animals store of copper in the liver.


Thiomolybdates only a concern in RUMINANT animals – only formed under reducing conditions in the rumen. Not formed in monogastric animals.

Cattle tolerance: 100 ppmPig tolerance: 450 ppmBreed and species differences exist

Symptoms of Cu chronic toxicity: Gradual build-up of Cu in liver up to 1000 ppm Acute release of Cu into blood Haemolytic crisis, renal and hepatic failure, death

ACUTE TOXICITY: In sheep death within 24-72 hours Nausea, salivation, abdominal pain, convulsions, paralysis, collapse Gastroenteritis, necrotic hepatitis, splenic and renal congestion

Treatment of mild Cu toxicity at early stages: Feed S and Mo to decopper ruminant animal Infuse thiomolybdate in monogastric animal

SELENIUM

Component of glutathione peroxidase present in a variety of tissues. Detoxifies peroxide radicals: (ROS) hydrogen peroxide, superoxides Prevents peroxidation damage to lipid membranes Protects unsaturated FA, including EFA Vitamin E relationship

Se absorption:Better for the organic forms:

Selenomethionine Selenocysteine

Less Available - Salts: Sodium Selenite Sodium Selenate

Excretion: Lungs, urine, feces

SELENIUM DEFICIENCY: (Same for Vit E deficiency)1. Nutritional muscular dystrophy - white muscle disease (lambs and calves)

2. Hepatosis dietetica - mulberry heart disease (pigs)

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Specific necrosis of cardiac muscle.


Tissue necrosis b/c of ROS. Deposition of collage and calcium salts cause white streaking


Vit E prevents oxidation of compounds (and thus prevents ROS production) Selenium/Glutathione peroxidase are curative (clean up ROS). High Vit E = lots of ROS generation Can then have less Se & GP because there will be less to clean up because of high Vit E.


Prone to reactions with ROS & can be extensively damaged. This include lipid membranes (Cell membrane damage = necrosis).


When combined w/ a transition metal (Cu, Fe, Mn) that is involved w/ donation or taking away electron. & generates hydroxyl radicals Called the fenton reaction.

3. Exudative diathesis - subcutaneous haemorrhages (chicks)

4. Infertility - retained placenta

Conditions: Low in soil, northern areas

Unavailable: Low pH, Fe complexing

Requirement: 0.25 - 0.50 ppmEnvironment: PUFA and Vit E content of diet influence requirement

Supplement: As Se salts in concentrate or free choice injectables

Focus on maternal nutrition to ensure adequate mineral status neonate

Se TOXICITY 10-15 fold safety range between requirement and toxicity

10-20 ppm for 8 weeks causes subacute toxicity in cattle

Se accumulator plants, e.g., milk vetch (loco weed)

1. Blind staggers / Alkali disease horses Sloughing of hoofs - lameness - deformation

2. Reduced fertility

3. Loss of long hair (horses)

Se S interactions in disulphide bonds proteins – there is constant competition b/w them. Need to consider sulfur content in prairies as a parameter to decide if we need to increase/decrease Se supplement.

PREVENTION:1. High inorganic sulphate intakes

2. High dietary protein levels

3. Arsenic supplements

VITAMIN/MINERAL NUTRITION

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In dairy cattle -

Critical to growth and health of animals. Grazing animals are of particular concern. It is important to know what role vitamins and minerals play in animal growth and physiology.

2 Types:

- Water Soluble Vitamins ( Thimin, Riboflavin, Niacin, Biotin, Folic Acid, Vit B12.

- Fat Soluble Vitamins (Vit A, E, D, K)

Groupinng of Vitamin and Minerals by Function.

Electrolytes (Na, K)Bones (Ca, P, Mg, Vit D, Vit K)Energy releasing vitamins (Thiamin, Riboflavin, Niacin, Biotin)Hematopoietic (Folate, B12, Fe, Cu)Antioxidant (Vit E, Vit C, Se, Vit A)Others (Vit A, I, Zn, Cr, Choline)

Vitamins: generally not synthesized by the body (when they are its from microbes) & must be supplied in the diet. These are organic nutrients required in small amounts for a variety of biochemical functions. Can account for some major diseases: scurvey, beriberi, rickets, pellagra.

First discovered vitamins (A and B) were fat and water soluble respectively.

Water Soluble – all absorbed by passive transport at high levels, and active transport at low levels (Except B12), excreted in the urine, toxicity rarely a problem, storage limited (Except B12 – in muscle). Vit C is good to prevent the common cold – but at high levels it can contribute to kidney stone formation.

Rumen bacteria can make B vitamins at levels that meet ruminant requirment.

In horses – can also make most B vitamins needed for their requirement so supplementation generally not needed.

Rabbits & Coprophagy – cecum fermentation – they reconsume soft feces that is high in microbial content – gives rabbit access to B-vitamins and microbial protein.

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Animal Nutrition - Small and Large Animals at WCVM

Health & Medicine

Transcript of Animal Nutrition - Small and Large Animals at WCVM