Lipid Metabolism

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Lipid Metabolism

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Essentially the metabolism of fatty acids and their derivatives

Hint 1

FA & derivatives

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Explain lipid Metab

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As the human body builds and renew its structures, obtains and stores energy and performs its various functions, there are numerous circumstances in which it is essential to use molecules or parts of molecules that do not associate with water.

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Classified as lipids

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Property of Lipids

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nonpolar and hydrophobic and is largely supplied by the substances classified as lipids

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Lipids

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Most of these are molecules that contain or are derived from fatty acids.

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1. Oxidation of FA - shown to be a major means of metabolic energy production, and it became clear that their storage in the form of TAGs was more efficient and quantitatively more important than storage of CHO as glycogen.

2. As details of the chemistry of biological structures were elucidated, hydrophobic structures were found to be largely composed of FA & their derivatives. Thus the major separation of cells and subcellular structures into separate aqueous compartments is accomplished by the use of membranes whose hydrophobic characteristics are largely supplied by the FA moieties of complex lipids such as phospholipids which are the most abundant lipid component of the cell membrane.

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Atleast 2 major roles of fatty acids and their derivatives in the human body

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1. Provide energy

2. Important component of cellular structures

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There are four (4) F H S D

Foods

Hydro

Synthesis

Degradat'n

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Sources of fatty acids

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1. Foods in te diet

2. Hydrolysis of stored TAG in the adipose tissue (lipolysis)

3. Synthesis of nutritionally nonessential fatty acid (lipogenesis)

4. Degradation of complex or compound lipids such as phospholipids and sphingolipids

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As foods they come in the form of butter, margarine, vegetable oils and animal fats.

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Triacylglycerol (TAGs)

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Most abundant lipid IN OUR DIET

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Remainder of dietary lipids

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Consist of cholesterol esters, phospholipids and unesterified fatty acids.

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Secreted by von Ebner's gland found at the back of the tongue.

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Lingual lipase

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First enzyme that acts on dietary Triacylglycerol.

Hint 9

This acid-stable lipase continue fat digestion in the stomach.

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Triacylglycerol

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Digestion of this lipid in the oral cavity is insignificant because of the very short stay of food in the mouth.

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These same TAGs are digested by an acid-stable gastric lipase secreted by the stomach mucosa.

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Short and medium chain FA esterified to TAGs

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Primary target of lingual lipase

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They are also important in individuals with cystic fibrosis who lack pancreatic lipase because of pancreatic insufficiency.

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Lingual lipase & Gastric lipase

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Cleave the primary ester bond in carbon 3 of Triacylglycerol and are important in neonates whose diet is made up primarily of milk fat.

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This highly efficient enzyme is primarily an alpha-esterase which cleaves the primary ester bonds found at carbons 1 and 3 in the Triacylglycerol molecule. However it cannot hydrolyze the secondary ester bond in the carbon 2, therefore the major end products of at digestion are 2-monoacylglycerol and free fatty acids.

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Pancreatic lipase - Steapsin

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The most important lipolysis enzyme in the digestive tract

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a) is acted upon by an intestinal enzyme isomerase converting it to 1- or 3- monoacylglycerol which is hydrolyzed by Steapsin to glycerol and free FA.

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2 major end products of fat digestion

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a) 2-monoacylglycerol and

b) FA

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Monoacylglycerol

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Poor substrates for hydrolysis so that less than 25% are completely digested

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Also neutralizes the INHIBITORY EFFECT of bile acids to Steapsin.

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Colipase

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Another protein

Also secreted by pancreas

Fxn: anchors pancreatic lipase at the lipid-aqueous interface thereby facilitating the release of free fatty acids.

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Colipase

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Also neutralizes the INHIBITORY EFFECT of bile acids to Steapsin.

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Orlistat

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An antiobesity drug that inhibits fat absorption by inhibiting

a) gastric lipase &

b) pancreatic lipase

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Role of (a) bile ACIDS and (b) bile SALTS in fat digestion and absorption

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a) become bile salts when conjugated with Glycine or Taurine in the liver BEFORE they are excreted into the bile canaliculi together with other constituents of bile

b) serve as emulsifying agent which breaks up big fat globules into smaller fat droplet emulsions thereby increasing the surface area of the TAg for enzymatic digestion by pancreatic lipase.

Also, together w/ phospholipids they form micelles w/c take up the products of fat digestion and bring them to the main site of lipid absorption, the brush border membrane of the intestinal mucosal cell (enterocyte). Very important in fat absorption.

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a) become bile salts when conjugated with Glycine or Taurine in the liver BEFORE they are excreted into the bile canaliculi together with other constituents of bile.

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Bile acids

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Carbon 24 steroids

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Cholic acid & Chenodeoxycholic acid

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Primary bile acids synthesized in the liver directly from cholesterol thru the action of 17-alpha hydroxylase.

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There are 2! Ca & Cdca :)

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Cholic acid & Chenodeoxycholic acid

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These are primary bile acids which become bile salts when conjugated with Glycine or Taurine in the liver BEFORE they are excreted into the bile canaliculi together with other constituents of bile.

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2 also! Da & Lca :)

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Primary bile acids

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Cholic acid & Chenodeoxycholic acid

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Secondary bile acids

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Deoxycholic acid & LITHOcholic acid

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Deoxycholic acid

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Secondary bile acid formed from CHOLIC acid

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Secondary bile acids

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LITHOcholic acid

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Secondary bile acid formed from Chedeoxycholic acid

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Deoxycholic acid & LITHOcholic acid

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Synthesized in the intestines through the action of bacterial enzyme.

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Principal role of bile salts in Fat digestion

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Serve as EMULSIFYING AGENT which breaks up big fat globules into smaller fat droplet emulsions thereby increasing the surface area of the Triacylglycerol for enzymatic digestion by pancreatic lipase.

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Another IMPT Fxn of bile SALTS

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together with Phospholipids they form MICELLES which take up the products of fat digestion and bring them to the main site of lipid absorption, the brush border membrane of the intestinal mucosal cell (enterocyte). Very important during fat absorption.

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Primary & Secondary bile acids

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Are conserved in the ILEUM by a process known as Enterohepatic circulation that resulted in their recycling and reutilization prior to their excretion thru the feces.

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Secondary bile acids

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are also conjugated with Glycine or Taurine in the liver cell so that practically the ones found in bile are the bile salts. This process is inhibited by the drug CHOLESTYRAMINE which binds bile acids in the lumen of the small intestine. This drug ALSO LOWERS the blood cholesterol level.

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CHOLESTYRAMINE

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Drug INHIBITOR of secondary bile acid process. It binds bile acid in the lumen of small intestine and ALSO LOWERS the blood cholesterol level.

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Digestion of other dietary lipids

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10-15% of dietary cholesterol is in esterified form. Cholesterol esters are hydrolyzed by cholesterol esterase to from free cholesterol and free fatty acid. Phosphoglycerides are digested by Phospholipase A2, a pancreatic enzyme, which removes the fatty acid from carbon 2 this forming lysophosphoglyveride (eg Lysolecithin). The remaining fatty acid in carbon 1 is removed by Lysophospholipase (Phospholipase B).

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10-15%

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Percentage of dietary cholesterol in esterified form.

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Cholesterol esters

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- are hydrolyzed by cholesterol esterase to form

1. Free cholesterol &

2. Free fatty acid

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Short & medium chain FA are absorbed by hepatic portal vein, transported in the blood by plasma albumin and delivered directly to the liver. 75% of 2-monoacylglycerols are esterified to long-chain FA via monoacylglycerol pathway to form long-chain TAG which are incorporated to chylomicron together with other dietary lipids. Chylomicron is absorbed by lacteals (lymphatic vessels) and passed on to the systemic blood via thoracic duct.

The fact that chylomicrons are absorbed by lymphatic circulation is a very good provision of nature because it prevents the development of fatty liver. This is so because chylomicron triglyceride is first hydrolyzed by extrahepatic lipoprotein to free FA and glycerol in the peripheral circulation before it goes to the liver as chylomicron remnant.

Most of the glycerol released from fat digestion in the small intestines are not reutilized but goes to the portal vein and then to the liver.

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Phosphoglycerides

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digested by Phospholipase A2, a pancreatic enzyme, which removes the FA from carbon 2 thus forming lysophosphoglycerine (eg Lysolecithin)

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Lysophospholipase

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a.k.a. Phospholipase B

It removes the remaining fatty acid in carbon 1 (digestion of other dietary lipid)

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Intestinal absorption of dietary lipids

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Short & medium chain FA are absorbed by hepatic portal vein, transported in the blood by plasma albumin and delivered directly to the liver. 75% of 2-monoacylglycerols are esterified to long-chain FA via monoacylglycerol pathway to form long-chain TAG which are incorporated to chylomicron together with other dietary lipids. Chylomicron is absorbed by lacteals (lymphatic vessels) and passed on to the systemic blood via thoracic duct.

The fact that chylomicrons are absorbed by lymphatic circulation is a very good provision of nature because it prevents the development of fatty liver. This is so because chylomicron triglyceride is first hydrolyzed by extrahepatic lipoprotein to free FA and glycerol in the peripheral circulation before it goes to the liver as chylomicron remnant.

Most of the glycerol released from fat digestion in the small intestines are not reutilized but goes to the portal vein and then to the liver.

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Short and medium-chain FA

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absorbed by the hepatic portal vein, transported in the blood by plasma albumin and delivered to the liver.

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75% of 2-monoacylglycerols

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are esterified to long-chain FA via monoacylglycerol pathway to form long-chain TAGs which are incorporated to chylomicron together with other dietary lipids.

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Chylomicron

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Absorbed by the lacteals (lymphatic vessels) and passed on to the systemic blood via the thoracic duct.

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Steatorrhea

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A clinical condition that results when fat digestion and/or absorption is impaired. It could be a part of malabsorption syndrome. It is characterized by the presence of increased amount of digested or undigested fats in the feces.

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Causes of Steatorrhea

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1. Deficiency of bile

2. Deficiency of pancreatic juice

3. Defect in intestinal mucosa

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Deficiency of bile

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This may be due to a complete obstruction in the common bile duct caused by a stone, structure or tumor. The stool is clay-colored because of the absence of bile pigment - Stercobilin. The stool may contain large amount of digested or undigested fats depending upon the site of obstruction in the common bile duct.

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Deficiency of pancreatic juice

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This may be due to pancreatic cancer or chronic pancreatitis. Feces contain large amount of undigested fats due to the absence or deficiency of pancreatic juice. The stool is normal in color.

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Defect in intestinal mucosa

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This could be caused by celiac disease (nontropical spruce or gluten-wheat enteropathy). Fat digestion is normal because there are pancreatic lipase and bile salts. The stool is characterized by the presence of large amount of digested but unabsorbed fats. Color of the stool is normal.

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LIPOGENESIS

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Fatty acid synthesis

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Fatty acids (FA)

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are synthesized when the diet is low in fat and/or high in CHO or CHON. Most are synthesized from dietary glucose.

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Liver

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Major site of lipogenesis or FA synthesis and to a lesser extent te adipose tissue.