Digestion Lecture Powerpoint

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© 2013 Pearson Education, Inc. Digestive Processes • Six essential activities 1.Ingestion 2.Propulsion 3.Mechanical breakdown 4.Digestion 5.Absorption 6.Defecation

Transcript of Digestion Lecture Powerpoint

Page 1: Digestion Lecture Powerpoint

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Digestive Processes

• Six essential activities1. Ingestion

2. Propulsion

3. Mechanical breakdown

4. Digestion

5. Absorption

6. Defecation

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Figure 23.2 Gastrointestinal tract activities.

Ingestion

Mechanicalbreakdown

Digestion

Propulsion

Absorption

Defecation

Food

PharynxEsophagus• Chewing (mouth)

• Swallowing (oropharynx)• Peristalsis (esophagus, stomach, small intestine, large intestine)

Stomach

Lymphvessel

Small intestineLargeintestine

Bloodvessel

Mainly H2OFeces

Anus

• Churning (stomach)• Segmentation (small intestine)

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GI Tract Regulatory Mechanisms

1. Mechanoreceptors and chemoreceptors – Respond to stretch, changes in osmolarity

and pH, and presence of substrate and end products of digestion

– Initiate reflexes that• Activate or inhibit digestive glands • Stimulate smooth muscle to mix and move lumen

contents

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GI Tract Regulatory Mechanisms

2. Intrinsic and extrinsic controls– Short reflexes - enteric nerve plexuses (gut

brain) respond to stimuli in GI tract– Long reflexes respond to stimuli inside or

outside GI tract; involve CNS centers and autonomic nerves

– Hormones from cells in stomach and small intestine stimulate target cells in same or different organs to secrete or contract

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Figure 23.4 Neural reflex pathways initiated by stimuli inside or outside the gastrointestinal tract.

External stimuli(sight, smell, taste,

thought of food)

Visceral afferents

Internal(GI tract)stimuli

Chemoreceptors,osmoreceptors, ormechanoreceptors

Long reflexes

Central nervous system

Local (intrinsic)nerve plexus("gut brain")

Effectors:Smooth muscle

or glands

Extrinsic visceral (autonomic)efferents

Short reflexes

Lumen of thealimentary canal

Gastrointestinalwall (site of shortreflexes)

Response:Change in

contractile orsecretory activity

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Gastric Gland Secretions

• Glands in fundus and body produce most gastric juice

• Parietal cell secretions– Hydrochloric acid (HCl)

pH 1.5–3.5 denatures protein, activates pepsin, breaks down plant cell walls, kills many bacteria

– Intrinsic factor• Glycoprotein required for absorption of vitamin B12

in small intestine

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Gastric Gland Secretions

• Chief cell secretions– Pepsinogen - inactive enzyme

• Activated to pepsin by HCl and by pepsin itself (a positive feedback mechanism)

– Lipases• Digest ~15% of lipids

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Gastric Gland Secretions

• Enteroendocrine cells– Secrete chemical messengers into lamina

propria• Act as paracrines

– Serotonin and histamine

• Hormones– Somatostatin (also acts as paracrine) and gastrin

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Mucosal Barrier

• Harsh digestive conditions in stomach

• Has mucosal barrier to protect– Thick layer of bicarbonate-rich mucus – Tight junctions between epithelial cells

• Prevent juice seeping underneath tissue

– Damaged epithelial cells quickly replaced by division of stem cells

• Surface cells replaced every 3–6 days

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Homeostatic Imbalance

• Gastritis– Inflammation caused by anything that

breaches mucosal barrier

• Peptic or gastric ulcers– Erosions of stomach wall

• Can perforate peritonitis; hemorrhage

– Most caused by Helicobacter pylori bacteria– Some by NSAIDs

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Figure 23.16 Photographs of a gastric ulcer and the H. pylori bacteria that most commonly cause it.

A gastric ulcer lesion H. pylori bacteria

Bacteria

Mucosalayer ofstomach

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Regulation of Gastric Secretion

• Neural and hormonal mechanisms

• Gastric mucosa up to 3 L gastric juice/day

• Vagus nerve stimulation secretion • Sympathetic stimulation secretion • Hormonal control largely gastrin

Enzyme and HCl secretion – Most small intestine secretions - gastrin

antagonists

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Regulation of Gastric Secretion

• Three phases of gastric secretion– Cephalic (reflex) phase – conditioned reflex

triggered by aroma, taste, sight, thought– Gastric phase – lasts 3–4 hours; ⅔ gastric

juice released• Stimulated by distension, peptides, low acidity,

gastrin (major stimulus)• Enteroendocrine G cells stimulated by caffeine,

peptides, rising pH gastrin

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Stimuli of Gastric Phase

• Gastrin enzyme and HCl release– Low pH inhibits gastrin secretion (as between meals)

• Buffering action of ingested proteins rising pH gastrin secretion

• Three chemicals - ACh, histamine, and gastrin - stimulate parietal cells through second-messenger systems– All three are necessary for maximum HCl secretion

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Regulation of Gastric Secretion

• Intestinal phase– Stimulatory component

• Partially digested food enters small intestine brief intestinal gastrin release

– Inhibitory effects (enterogastric reflex and enterogastrones)

• Chyme with H+, fats, peptides, irritating substances inhibition

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Enterogastric Reflex

• Three reflexes act to– Inhibit vagal nuclei in medulla– Inhibit local reflexes– Activate sympathetic fibers tightening of

pyloric sphincter no more food entry to small intestine

Decreased gastric activity protects small intestine from excessive acidity

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Intestinal Phase

• Enterogastrones released– Secretin, cholecystokinin (CCK),

vasoactive intestinal peptide (VIP)• All inhibit gastric secretion

• If small intestine pushed to accept more chyme dumping syndrome– Nausea and vomiting– Common in gastric reduction for weight loss

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Figure 23.17 Neural and hormonal mechanisms that regulate release of gastric juice.

Lack ofstimulatoryimpulses toparasym-patheticcenter

Gastrinsecretiondeclines

Overridesparasym-patheticcontrols

Sympatheticnervoussystemactivation

Cerebralcortex

G cells

Emotionalstress

Excessiveacidity(pH < 2)in stomach

Loss ofappetite,depression

Entero-gastricreflex

Localreflexes

Pyloricsphincter

Vagalnucleiin medulla

Distensionof duodenum;presence offatty, acidic, orhypertonicchyme; and/orirritants inthe duodenum

Release ofenterogastrones(secretin, cholecystokinin,vasoactive intestinalpeptide)

Distension;presence offatty, acidic,partiallydigested foodin theduodenum

Intestinal(enteric)gastrinreleaseto blood

Briefeffect

Gastrinreleaseto blood

Vagusnerve

Vagusnerve

Conditioned reflex

Localreflexes

Vagovagalreflexes

G cells

Presence ofpartially digested foods in duodenumor distension of theduodenum when stomach begins to empty

Stimulate

Inhibit

Hypothalamusand medullaoblongata

Cerebral cortex

Medulla Stomachdistensionactivatesstretchreceptors

Food chemicals(especially peptides andcaffeine) and rising pHactivate chemoreceptors

Stimulation oftaste and smellreceptors

Sight and thoughtof food

1

1

2

1

2

1

2

1

2

1

Stimulatory events Inhibitory events

Cephalicphase

Gastricphase

Intestinalphase

Stomachsecretoryactivity

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Response of the Stomach to Filling

• Stretches to accommodate incoming food– Pressure constant until 1.5 L food ingested

• Reflex-mediated receptive relaxation– Coordinated by swallowing center of brain stem

– Gastric accommodation• Plasticity (stress-relaxation response) of smooth

muscle (see Chapter 9)

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Gastric Contractile Activity

• Peristaltic waves move toward pylorus at rate of 3 per minute – Basic electrical rhythm (BER) set by enteric

pacemaker cells (formerly interstitial cells of Cajal)

– Pacemaker cells linked by gap junctions entire muscularis contracts

• Distension and gastrin increase force of contraction

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Figure 23.19 Deglutition (swallowing). Slide 1

Pyloricvalveclosed

Pyloricvalveslightlyopened

Pyloricvalveclosed

Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus.

Retropulsion: The pyloric end of the stomach acts as a pump that delivers small amounts of chyme into the duodenum, simultaneously forcing most of its contained material backward into the stomach.

2 Propulsion: Peristaltic waves move from the fundus toward the pylorus.

1 3

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Regulation of Gastric Emptying

• As chyme enters duodenum– Receptors respond to stretch and chemical

signals– Enterogastric reflex and enterogastrones

inhibit gastric secretion and duodenal filling

• Carbohydrate-rich chyme moves quickly through duodenum

• Fatty chyme remains in duodenum 6 hours or more

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Presence of fatty, hypertonic,acidic chyme in duodenum

Duodenal entero-endocrine cells

Chemoreceptors andstretch receptors

Secrete Target

Enterogastrones(secretin, cholecystokinin,vasoactive intestinalpeptide)

Via shortreflexes

Via longreflexes

Duodenalstimulidecline

Entericneurons

CNS centers sympathetic activity; parasympathetic activity

Contractile force andrate of stomachemptying decline

Initial stimulus Stimulate

Inhibit

Figure 23.20 Neural and hormonal factors that inhibit gastric emptying.

Physiological response

Result

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Regulation of Bile Secretion

• Bile secretion stimulated by– Bile salts in enterohepatic circulation – Secretin from intestinal cells exposed to HCl

and fatty chyme

• Hepatopancreatic sphincter closed unless digestion active bile stored in gallbladder– Released to small intestine ~ only with

contraction

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Regulation of Bile Secretion

• Gallbladder contraction stimulated by– Cholecystokinin (CCK) from intestinal cells

exposed to acidic, fatty chyme– Vagal stimulation (minor stimulus)

• CCK also causes– Secretion of pancreatic juice – Hepatopancreatic sphincter to relax

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Regulation of Pancreatic Secretion

• CCK induces secretion of enzyme-rich pancreatic juice by acini

• Secretin causes secretion of bicarbonate-rich pancreatic juice by duct cells

• Vagal stimulation also causes release of pancreatic juice (minor stimulus)

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Figure 23.28 Mechanisms promoting secretion and release of bile and pancreatic juice. Slide 1

Chyme enter-ing duodenum causes duodenalenteroendocrine cells to release cholecystokinin(CCK) and secretin.

CCK (red dots) andsecretin (yellow dots) enter the bloodstream.

CCK inducessecretion of enzyme-richpancreatic juice. Secretin causes secretion of HCO3

− -rich pancreatic juice.

Bile salts and, to a lesser extent, secretintransported viabloodstream stimulate Liver to produce bile more rapidly.

CCK (via blood stream) causes gallbladder to contract and HepatopancreaticSphincter to relax. Bile Enters duodenum. During cephalicand gastric phases,vagal Nerve stimu-lates gallbladder tocontract weakly.

CCK secretion

Secretin secretion

1

2

3

4

5

6

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Digestion in the Small Intestine

• Chyme from stomach contains– Partially digested carbohydrates and proteins – Undigested fats

• 3–6 hours in small intestine– Most water absorbed– ~ All nutrients absorbed

• Small intestine, like stomach, no role in ingestion or defecation

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Requirements for Digestion and Absorption in the Small Intestine

• Slow delivery of acidic, hypertonic chyme

• Delivery of bile, enzymes, and bicarbonate ions from liver and pancreas

• Mixing

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Motility of the Small Intestine

• Segmentation– Most common motion of small intestine– Initiated by intrinsic pacemaker cells – Mixes/moves contents toward ileocecal valve– Intensity altered by long & short reflexes;

hormones• Parasympathetic ; sympathetic

– Wanes in late intestinal (fasting) phase

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Motility of the Small Intestine

• Peristalsis– Initiated by rise in hormone motilin in late

intestinal phase; every 90–120 minutes – Each wave starts distal to previous

• Migrating motor complex

– Meal remnants, bacteria, and debris moved to large intestine

– From duodenum ileum ~ 2 hours

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Figure 23.3a Peristalsis and segmentation.

Frommouth

Peristalsis: Adjacent segments of alimentary tract organs alternately contract and relax, moving food along the tract distally.

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Motility of the Small Intestine

• Local enteric neurons coordinate intestinal motility

• Cholinergic sensory neurons may activate myenteric plexus– Causes contraction of circular muscle

proximally and of longitudinal muscle distally– Forces chyme along tract

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Motility of the Small Intestine

• Ileocecal sphincter relaxes, admits chyme into large intestine when– Gastroileal reflex enhances force of

segmentation in ileum– Gastrin increases motility of ileum

• Ileocecal valve flaps close when chyme exerts backward pressure– Prevents regurgitation into ileum

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Digestion

• Digestion– Catabolic; macromolecules monomers

small enough for absorption

• Enzymes– Intrinsic and accessory gland enzymes break

down food

• Hydrolysis– Water is added to break bonds

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Digestion of Carbohydrates

• Only monosaccharides can be absorbed

• Monosaccharides absorbed as ingested– Glucose, fructose, galactose

• Digestive enzymes– Salivary amylase, pancreatic amylase, and

brush border enzymes (dextrinase, glucoamylase, lactase, maltase, and sucrase)

– Break down disaccharides sucrose, lactose, maltose; polysaccharides glycogen and starch

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Digestion of Carbohydrates

• Starch digestion– Salivary amylase (saliva) oligosaccharides

at pH 6.75 – 7.00– Pancreatic amylase (small intestine)

breaks down any that escaped salivary amylase oligosaccharides

– Brush border enzymes (dextrinase, glucoamylase, lactase, maltase, sucrase) oligosaccharides monosaccharides

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Figure 23.32 Flowchart of digestion and absorption of foodstuffs. (1 of 4)

Foodstuff Enzyme(s) and source Site of action Path of absorption

Starch and disaccharides

Oligosaccharidesand disaccharides

Carbohydratedigestion

Lactose Maltose Sucrose

Galactose Glucose Fructose

Salivary amylase

Pancreatic amylase

Brush border enzymes in small intestine(dextrinase, gluco-amylase, lactase, maltase, and sucrase)

Mouth

Small intestine

Small intestine

• Glucose and galactose are absorbed via cotransport with sodium ions.• Fructose passes via facilitated diffusion.• All monosaccharides leave the epithelial cells via facilitated diffusion, enter the capillary blood in the villi, and are transported to the liver via the hepatic portal vein.

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Digestion of Proteins

• Source is dietary, digestive enzymes, mucosal cells; digested to amino acid monomers

• Begins with pepsin in stomach at pH 1.5 – 2.5– Inactive in high pH of duodenum

• Pancreatic proteases– Trypsin, chymotrypsin, and carboxypeptidase

• Brush border enzymes– Aminopeptidases, carboxypeptidases, and

dipeptidases

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Figure 23.33 Protein digestion and absorption in the small intestine. Slide 1Lumen of intestine

Pancreaticproteases

Amino acids of protein fragments

Brush border enzymes

Na+

Absorptiveepithelialcell

Apical membrane (microvilli)

Aminoacidcarrier

Capillary

Proteins and protein fragments are digested to amino acids by pancreatic proteases (trypsin, chymotrypsin, and carboxy- peptidase), and by brush border enzymes (carboxypeptidase, aminopeptidase, and dipeptidase)of mucosal cells.

The amino acids are then absorbed by active transport into the absorptive cells, and move to their opposite side.

The amino acids leave the villus epithelial cell by facilitated diffusion and enter the capillary viaintercellular clefts.

Na+

1

2

3

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Figure 23.33 Protein digestion and absorption in the small intestine. Slide 2Lumen of intestine

Pancreaticproteases

Amino acids of protein fragments

Brush border enzymes

Na+

Absorptiveepithelialcell

Apical membrane (microvilli)

Capillary

Proteins and protein fragments are digested to amino acids by pancreatic proteases (trypsin, chymotrypsin, and carboxy- peptidase), and by brush border enzymes (carboxypeptidase, aminopeptidase, and dipeptidase)of mucosal cells.

Na+

1

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Figure 23.33 Protein digestion and absorption in the small intestine. Slide 3Lumen of intestine

Pancreaticproteases

Amino acids of protein fragments

Brush border enzymes

Na+

Absorptiveepithelialcell

Apical membrane (microvilli)

Aminoacidcarrier

Capillary

Proteins and protein fragments are digested to amino acids by pancreatic proteases (trypsin, chymotrypsin, and carboxy- peptidase), and by brush border enzymes (carboxypeptidase, aminopeptidase, and dipeptidase)of mucosal cells.

The amino acids are then absorbed by active transport into the absorptive cells, and move to their opposite side.

Na+

1

2

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Figure 23.33 Protein digestion and absorption in the small intestine. Slide 4Lumen of intestine

Pancreaticproteases

Amino acids of protein fragments

Brush border enzymes

Na+

Absorptiveepithelialcell

Apical membrane (microvilli)

Aminoacidcarrier

Capillary

Proteins and protein fragments are digested to amino acids by pancreatic proteases (trypsin, chymotrypsin, and carboxy- peptidase), and by brush border enzymes (carboxypeptidase, aminopeptidase, and dipeptidase)of mucosal cells.

The amino acids are then absorbed by active transport into the absorptive cells, and move to their opposite side.

The amino acids leave the villus epithelial cell by facilitated diffusion and enter the capillary viaintercellular clefts.

Na+

1

2

3

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Figure 23.32 Flowchart of digestion and absorption of foodstuffs. (2 of 4)

Proteindigestion

Proteins

Large polypeptides

Small polypeptides,small peptides

Amino acids(some dipeptidesand tripeptides)

Pepsin (stomach glands)in presence of HCl

Pancreaticenzymes (trypsin, chymotrypsin,carboxypeptidase)

Brush border enzymes(aminopeptidase,carboxypeptidase,and dipeptidase)

Stomach

Small intestine

Small intestine

• Amino acids are absorbed via cotransport with sodium ions.• Some dipeptides and tripeptides are absorbed via cotransport with H+ and hydrolyzed to amino acids within the cells.• Infrequently, transcytosis of small peptides occurs.• Amino acids leave the epithelial cells by facilitated diffusion, enter the capillary blood in the villi, and are transported to the liver via the hepatic portal vein.

Foodstuff Enzyme(s) and source Site of action Path of absorption

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Digestion of Lipids

• Pre-treatment—emulsification by bile salts– Does not break bonds

• Enzymes—pancreatic lipases Fatty acids and monoglycerides

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Fat globule

Bile salts in the duodenum emulsify large fat globules (physically break them up into smaller fat droplets).

Digestion of fat by the pancreatic enzyme lipase yields free fatty acids and monoglycerides. These then associate with bile salts to form micelles which “ferry” them to the intestinal mucosa.

Micelles made up of fatty acids,monoglycerides, and bile salts

Bile salts

Fat dropletscoated withbile salts

Fatty acids and monoglycerides leave micelles and diffuse into epithelial cells. There they are recombined and packaged with other fatty substances and proteins to form chylomicrons.

Chylomicrons are extruded from the epithelial cells by exocytosis. The chylomicrons enter lacteals and are carried away from the intestine in lymph.

Lacteal

Epithelialcells ofsmallintestine

1

2

3

4

Figure 23.34 Emulsification, digestion, and absorption of fats. Slide 1

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Figure 23.32 Flowchart of digestion and absorption of foodstuffs. (3 of 4)

Fat digestion

Unemulsified triglycerides

Lingual lipase

Gastric lipase

Emulsification by the detergent action of bile salts ductedin from the liver

Pancreatic lipases

Monoglycerides (or diglycerideswith gastric lipase) and fatty acids

Mouth

Stomach

Small intestine

Small intestine

• Fatty acids and monoglycerides enter the intestinal cells via diffusion. • Fatty acids and monoglycerides are recombined to form triglycerides and then combined with other lipids and proteins within the cells. The resulting chylomicrons are extruded by exocytosis.• The chylomicrons enter the lacteals of the villi and are transported to the systemic circulation via the lymph in the thoracic duct.• Some short-chain fatty acids are absorbed, move into the capillary blood in the villi by diffusion, and are transported to the liver via the hepatic portal vein.

Foodstuff Enzyme(s) and source Site of action Path of absorption

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Digestion of Nucleic Acids

• Enzymes– Pancreatic ribonuclease and

deoxyribonuclease nucleotide monomers– Brush border enzyme nucleosidases and

phosphatases free bases, pentose sugars, phosphate ions

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Figure 23.32 Flowchart of digestion and absorption of foodstuffs. (4 of 4)

Nucleic aciddigestion

Nucleic acids

Pentose sugars, N-containing bases,

phosphate ions

Pancreatic ribo-nuclease and deoxyribonuclease

Brush borderenzymes(nucleosidasesand phosphatases)

Small intestine

Small intestine

• Units enter intestinal cells by active transport via membrane carriers.• Units are absorbed into capillary blood in the villi and transported to the liver via the hepatic portal vein.

Foodstuff Enzyme(s) and source Site of action Path of absorption

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Absorption

• ~ All food; 80% electrolytes; most water absorbed in small intestine– Most prior to ileum

• Ileum reclaims bile salts

• Most absorbed by active transport blood– Exception - lipids

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Absorption of Carbohydrates

• Glucose and galactose– Secondary active transport (cotransport) with

Na+ epithelial cells– Move out of epithelial cells by facilitated

diffusion capillary beds in villi

• Fructose– Facilitated diffusion to enter and exit cells

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Absorption of Carbohydrates

• Glucose and galactose– Secondary active transport (cotransport) with

Na+ epithelial cells– Move out of epithelial cells by facilitated

diffusion capillary beds in villi

• Fructose– Facilitated diffusion to enter and exit cells

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Absorption of Protein

• Amino acids transported by several types of carriers– Most coupled to active transport of Na+

• Dipeptides and tripeptides actively absorbed by H+-dependent cotransport; digested to amino acids within epithelial cells

• Enter capillary blood by diffusion

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Homeostatic Imbalance

• Whole proteins not usually absorbed

• Can be taken up by endocytosis/exocytosis– Most common in newborns food allergies

• Usually disappear with mucosa maturation

– Allows IgA antibodies in breast milk to reach infant's bloodstream passive immunity

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Absorption of Lipids

• Absorption of monoglycerides and fatty acids– Cluster with bile salts and lecithin to form micelles– Released by micelles to diffuse into epithelial cells– Combined with lecithin, phospholipids, cholesterol, &

coated with proteins to form chylomicrons– Enter lacteals; transported to systemic circulation– Hydrolyzed to free fatty acids and glycerol by

lipoprotein lipase of capillary endothelium• Cells can use for energy or stored fat

• Absorption of short chain fatty acids– Diffuse into portal blood for distribution

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Absorption of Nucleic Acids

• Absorption– Active transport across epithelium

bloodstream

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Absorption of Vitamins

• In small intestine– Fat-soluble vitamins (A, D, E, and K) carried

by micelles; diffuse into absorptive cells– Water-soluble vitamins (vitamin C and B

vitamins) absorbed by diffusion or by passive or active transporters.

– Vitamin B12 (large, charged molecule) binds with intrinsic factor, and is absorbed by endocytosis

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Absorption of Vitamins

• In large intestine– Vitamin K and B vitamins from bacterial

metabolism are absorbed

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Absorption of Electrolytes

• Most ions actively along length of small intestine• Iron and calcium are absorbed in duodenum • Na+ coupled with active absorption of glucose

and amino acids• Cl– transported actively• K+ diffuses in response to osmotic gradients; lost

if poor water absorption• Usually amount in intestine is amount absorbed

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Absorption of Electrolytes

• Iron and calcium absorption related to need– Ionic iron stored in mucosal cells with ferritin– When needed, transported in blood by

transferrin

• Ca2+ absorption regulated by vitamin D and parathyroid hormone (PTH)

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Absorption of Water

• 9 L water, most from GI tract secretions, enter small intestine– 95% absorbed in the small intestine by

osmosis– Most of rest absorbed in large intestine

• Net osmosis occurs if concentration gradient established by active transport of solutes

• Water uptake coupled with solute uptake

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Malabsorption of Nutrients

• Causes– Anything that interferes with delivery of bile or

pancreatic juice – Damaged intestinal mucosa (e.g., bacterial

infection; some antibiotics)

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Malabsorption of Nutrients

• Gluten-sensitive enteropathy (celiac disease)– Immune reaction to gluten– Gluten causes immune cell damage to

intestinal villi and brush border– Treated by eliminating gluten from diet (all

grains but rice and corn)