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Section VI. Lipid Metabolism Section VI. Lipid metabolism overview: Major categories of lipids (not very water-soluble): Fatty acids and triagylclycerol.

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Presentation on theme: "Section VI. Lipid Metabolism Section VI. Lipid metabolism overview: Major categories of lipids (not very water-soluble): Fatty acids and triagylclycerol."— Presentation transcript:

1 Section VI. Lipid Metabolism Section VI. Lipid metabolism overview: Major categories of lipids (not very water-soluble): Fatty acids and triagylclycerol (TG) Glycerophospholipids and sphingolipids Eicosanoids (prostaglandins, thromboxanes) Cholesterol, bile salts, steroid hormones Fat-soluble vitamins (A, D, E, K) Triacylglycerol

2 Overview Fatty acid metabolism Fatty acid metabolism: (Chapts. 32, 33) Fatty acids can be dietary or synthesized in liver Can be oxidized for energy → CO 2 and H 2 O Can be stored as triacylglycerol in adipose tissue Can be used to make phospholipids and sphingolipids for membrane components

3 Overview of cholesterol metabolism Cholesterol metabolism (chapt. 34): Is incorporated into membranes for stability Is a precursor for bile salts (gall bladder secretes) Is a precursor for steroid hormones

4 Overview lipoprotein particles in blood Lipoprotein particles transport lipids in blood: Triacylglycerol is major dietary lipid: Digested in intestinal lumen: free FA and 2-mono- acylglycerol are reconverted to TG in intestinal cells TG are packaged as chylomicrons (apoB) and secreted into blood ; matured with additional proteins VLDL (very-low-density-lipoproteins) produced in liver from dietary carbohydrates (insulin stimulated) Lipoprotein lipase (LPL) on cells degrades the lipoproteins; FA into cells HDL (high-density-lipoproteins) transport excess cholesterol to liver; exchange proteins

5 Lipid metabolism overview Triacylglycerol metabolism: Fed state: TG digested to 2-MG and FA, into intestinal cells TG reform (chylomicrons) with protein, into blood Liver forms VLDL by lipogenesis from sugars VLDL donates protein to chylomicron, which binds LPL on cells and is cleaved to release FA into muscle, adipose Fasting state: Fatty acids, glycerol released from adipose Glycerol used for gluconeogenesis liver FA used for ketone bodies, or oxidation (muscles, other )

6 Chapt. 32 Ch. 32 Digestion and Transport of Dietary Lipids Student Learning Outcomes : Explain digestion of triacylglycerols (TG) to free fatty acids (FA) and 2-monoacylglycerol (2-MG) Describe the role of bile salts in this process Describe how micelles enter epithelial cells, and are reconverted to TG Explain how TG plus apoproteins and other lipids form nascent chylomicrons that exit cells Describe role of HDL lipoproteins to mature the nascent chylomicrons, and breakdown of particles

7 I. Digestion of dietary triacylglycerols Major fat in diet (storage of lipids plants, animals) Lipases digest to 2-monoacylglycerol (2-MG) Bile salts emulsify fat in small intestine Bile salts derived from cholesterol Fig. 1 fatty acids in triacylglycerol Fig. 2, a bile salt

8 Digestion, absorption Fig. 3:TG, triacylglycerol; BS, bile salt, FA, fatty acid 2-MG, 2-monoacylglycerol Digestion of dietary triacylglycerols: Lipases digest Bile salts emulsify, colipases aid lipases TG reform in epithelium

9 Enzymes degrade lipids Enzymes degrade lipids: Lipases cleave C1, C3 of TG Cholesterol esterase removes FA Phospholipase degrades phospholipid Figs. 5,6

10 Absorption Figs. 3,6 Absorption into intestinal epithelial cells: FA, 2-MG, cholesterol, other lipids, BS in micelles Lipids absorbed through microvilli, not bile salts Bile salts are recycled Short, med-chain FA absorb directly epithelium, enter bloodstream bound to serum albumin

11 III. Chylomicrons TG are resynthesized in intestinal epithelia ATP activates FA → FA-CoA (in Smooth ER) Apoproteins and other lipids bind [ synthesis of TG in liver, adipose starts with phosphatidic acid] Fig. 7

12 Blood lipoproteins Blood lipoprotein particles transport lipids: Chylomicrons – produced in intestinal cells from dietary fat; carry TG in blood VLDL – produced from liver mainly from dietary carbohydrate; carries TG in blood IDL - produced in blood (remnant of VLDL) LDL – produced in blood (remnant of IDL after TG digestion; high concentration of cholesterol; endocytosed by liver, other tissues (LDL receptor) HDL – produced in liver, intestine; exchanges proteins and lipids with other lipoproteins; returns cholesterol to liver

13 Transport of lipids in blood Transport of lipids uses lipoprotein complexes: Lipids are not soluble in water; would coalesce Phospholipids, protein on outside; hydrophobic inside Cholesterol esters have fatty acid moiety Ex. VLDL from liver (very-low density lipoprotein) Fig. 8 Fig. 33.10

14 Nascent Chylomicrons Figs. 9,10 Nascent chylomicrons from dietary TG: SER enzymes reform the TG Least dense lipoproteins (lot of TG) Proteins made on RER Apoprotein B-48

15 Fig. 11 Apoprotein B gene B-apoprotein gene encodes two polypeptides: ApoB-100 in liver VLDL particles ApoB-48 in intestinal cells is only 48% length RNA editing changed codon in mRNA

16 IV. Lipoprotein particles transport dietary lipids in blood Additional proteins form mature chylomicrons: ‘Nascent chylomicrons’ exocytosed into blood Acquire additional proteins from HDL particles ApoCII binds enzyme LPL on cell surfaces Lipoprotein lipases ApoE binds receptor on liver cell for recycling Fig. 12

17 Fate of chylomicrons Fig. 13 Chylomicrons from dietary lipids: matured in blood by HDL particle interaction Are digested at capillary wall by LPL (CII activates) Insulin stimulates more LPL on surface FA binds albumin in blood FA into muscle (energy) FA into adipose (store) Remnants bind liver through ApoE-receptor Recycled in lysosome

18 Olestra Olestra is artificial fat substitute Tastes like fat, not metabolized sucrose with fatty acyl groups esterified on OH resistant to hydrolysis by lipases, passes through carries lipid-soluble vitamins

19 Key concepts: Triacylglycerols are major fat source in diet Lipases perform digestion, bile salts emulsify Free fatty acids and 2-monoacylglycerol form Micelles transport components into intestinal cells Nascent chylomicrons are reformed from TG, cholesterol and apoB-48 protein; pass into blood HDL particles contribute additional proteins to form mature chlymicrons LPL (lipoprotein lipase) on cell surface cleaves TG and cells gain FA; remnants recycled in liver

20 Review question Type III hyperlipidemia is caused by a deficiency of apoprotein E. Analysis of the serum of patients with this disorder would exhibit which of the following? a.An absence of chylomicrons after eating b.Above-normal levels of VLDL after eating c.Normal triglyceride levels d.Elevated triglyceride levels e.Below-normal triglyceride levels

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