Chemistry 2100

Chapter 21

Lipids

Fatty Acids

COOH

oleic acid (mp 4°C)

stearic acid (mp 70°C)

COOH

Triacylglycerols

Fatty Acids

The fatty acid components of triglycerides have certain

things in common:

1. Practically all are unbranched carboxylic acids.

2. They range in size from about 10 to 20 carbons.

3. They contain an even number of carbon atoms.

4. Apart from the –COOR ester groups, triglycerides have no functional groups, except that some have one or more carbon-carbon double bonds in the fatty acid hydrocarbon chains.

5. In most fatty acids that have carbon-carbon double

bonds, the cis isomers predominate.

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Saponification• Saponification: the base-promoted hydrolysis of fats

and oils in aqueous NaOH and produces glycerol and a mixture of fatty acid salts called soaps.

O

CH2OCR

CH2OCR

RCOCH

O

O

CH2OH

CH2OH

HOCH RCO-Na+O

A triglyceride 1,2,3-Propanetriol(Glycerol, glycerin)

+

Sodium soaps

3saponification

anionic detergents

(-HOH)

so dium la ury l sulfa te

S

O

O

O NaCH3CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2CH2O

N a OHH2SO4CH3(CH2)1 0CH2O S

O

O

OHCH3(CH2)1 0CH2OH

la ury l a lco ho l

Synthetic Detergents (syndets)

Hydrogenation

Hardening: The reduction of some or all of the carbon-carbon double bonds of an unsaturated triglyceride using H2/transition metal catalyst, which converts a liquid triglyceride to a semisolid.

"partially hydrogenated vegetable oil"

+

COOH

COOH

COOH

H2 cata lyst

• •

Complex Lipids

Membranes: Glycerophospholipids

Fluid Mosaic Model

Figure 21.2 The fluid mosaic model of membranes.

O

O

O

O

Other Lipids: Waxes

Sterols

Steroids RU-486

O

HO

C C CH3

Me2N

cholesterol

HO

progesterone

O

O testosterone

O

OH

estradiol

HO

OH

Bile Salts

Bile salts are oxidation products of cholesterol.• Synthesized in the liver, stored in the gallbladder, and

secreted into the intestine where they emulsify dietary fats and aid in their absorption and digestion.

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Low-Density Lipoprotein

Cholesterol Transport

– Transport of cholesterol from the liver starts out as a large VLDL particle.

– VLDL is carried in the serum.– As fat is removed, its density increases and it

becomes LDL; LDL stays in the plasma for about 2.5 days.

– LDL carries cholesterol to cells, where specific LDL receptors bind it.

– After binding, LDL is taken into cells where enzymes liberate free cholesterol and cholesteryl esters.

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Cholesterol Transport

– High-density lipoproteins (HDL) transport cholesterol from peripheral tissues to the liver and also transfer cholesterol to LDL.

– While in the serum, free cholesterol in HDL is converted to cholesteryl esters.

– In the liver, HDL binds to the liver cell surface and transfers its cholesteryl esters to the cell.

– These esters are used for the synthesis of steroid hormones and bile acids.

– After HDL has delivered its cholesteryl esters to liver cells, it reenters circulation.

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Levels of LDL and HDL

– Most of the cholesterol is carried by LDL.– Normal plasma levels are 175 mg/100 mL.– If there are sufficient LDL receptors on the surface of

cells, LDL is removed from circulation and its concentration in blood plasma drops.

– The number of LDL receptors is controlled by a feedback mechanism.

– When the concentration of cholesterol inside cells is high, the synthesis of LDL receptors is suppressed.

– In the disease called famelial hypercholesterolemia, there are not enough LDL receptors and plasma levels of cholesterol may rise as high as 680 mg/100 mL.

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Levels of LDL and HDL– These high levels of cholesterol can cause premature

atherosclerosis and heart attacks.– In general, high LDL means high cholesterol content in the

plasma because LDL cannot get into cells.– Therefore, high LDL together with low HDL is a symptom of faulty

cholesterol transport and a warning of possible atherosclerosis.– The serum cholesterol level controls cholesterol synthesis in the

liver.– When serum cholesterol is high, its synthesis in the liver is low,

and vice versa.– The commonly used statin drugs inhibit the synthesis of

cholesterol by blocking HMG-CoA reductase.

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Prostaglandins

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COX Enzymes

• The COX (cyclooxygenase) enzyme occurs in two forms:

• COX-1 catalyzes the normal physiological production of prostaglandins.

• COX-2 is responsible for the production of prostaglandins in inflammation.– When a tissue is injured or damaged, special

inflammatory cells invade the injured tissue and interact with resident cells, for example, smooth muscle cells.

– This interaction activates COX-2 and prostaglandins are synthesized.

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Thromboxanes

Thromboxanes are also derived from arachidonic acid.– Thromboxane A2 induces platelet aggregation and

vasoconstriction.– Aspirin and other NSAIDs inhibit the synthesis of

thromboxanes by inhibiting the COX enzyme.

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Leukotrienes

Leukotrienes are also synthesized from arachidonic acid.– They occur mainly in leukocytes.– They produce muscle contractions, especially in the

lungs and thereby can cause asthma-like attacks. They are 100x more potent than histamine.

– Several recently-developed anti-asthma drugs inhibit the synthesis of leukotrienes.

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