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Basics of Lipid And Lipoprotein Metabolism PowerPoint Presentation

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Description : Check out this medical titled "Basics of Lipid and Lipoprotein Metabolism" by John R. Guyton, MD.

This medical talks about lipid and lipoprotein metabolism.

Lipids are a diverse group of biomolecules that play many essential roles in the human body, including energy storage, membrane structure, and cell signaling. Lipids include fatty acids, triglycerides, phospholipids, and cholesterol.

Lipid metabolism refers to the processes by which lipids are synthesized, transported, and degraded in the body. Lipoproteins are complexes of lipids and proteins that transport lipids in the blood.

The liver plays a central role in lipid metabolism. It synthesizes lipids, including cholesterol and triglycerides, and converts excess dietary carbohydrates into fatty acids and then into triglycerides for storage in adipose tissue. The liver also converts excess amino acids into urea and glucose.

Lipoproteins are classified according to their density, which reflects the amount of lipid they contain. The major lipoproteins are chylomicrons, very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL).

Chylomicrons are the largest and least dense lipoproteins and are formed in the small intestine after the ingestion of dietary fat. They transport dietary triglycerides to adipose tissue for storage or to muscle cells for energy use.

VLDL is produced in the liver and transports endogenous triglycerides to adipose tissue for storage. As VLDLs lose triglycerides, they become denser and eventually become LDLs.

LDLs are the main carriers of cholesterol in the blood and are sometimes called "bad" cholesterol because high levels are associated with an increased risk of cardiovascular disease. HDLs are smaller and denser than LDLs and are sometimes called "good" cholesterol because they remove excess cholesterol from the blood and transport it back to the liver for excretion.

Overall, lipid and lipoprotein metabolism are essential for maintaining the health of the body, but imbalances in lipid metabolism can lead to various health problems, including heart disease, stroke, and obesity.

Tags : lipid and lipoprotein metabolism, biomolecules, Lipid metabolism, chylomicrons, very-low-density lipoproteins, low-density lipoproteins, endocrinology, endocrinology

Published on : Apr 21, 2023 | Views : 1826 | Downloads : 5

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Basics of Lipid andLipoprotein Metabolism John R. Guyton, M.D. Associate Professor of Medicine Duke University Durham, NC
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Lipid Structure HO Cholesterol COOH COOH COOH HO HO HO + Fatty Acids Glycerol COO COO COO Triglycerides COO COO OPOO N Phospholipid: Lecithin +
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HMG CoA Reductase (More Than Cholesterol Synthesis) Acetyl CoA HMG CoA Mevalonate Farnesyl Pyrophosphate Cholesterol HMG CoA Reductase Isopentenyl adenine (transfer RNA) Prenylation of signalling peptides (ras, rho, etc.) Ubiquinones (CoQ-10, etc.) Dolichols Inhibition of other key products of mevalonate may relate to nonlipid effects & rare side effects of statins.
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NORMAL CHOLESTEROL METABOLISM 0.8 G SYN CHOL* *SYN CHOL = CHOLESTEROL SYNTHESIS 0.4 G CHOL
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NORMAL CHOLESTEROL METABOLISM .65 G .20 G .20 G CHOL 0.65 G CHOL 0.85 G ABS CHOL 50% 0.4 G CHOL 0.8 G SYN CHOL* *SYN CHOL = CHOLESTEROL SYNTHESIS 1.3 G CHOL
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Key concepts: synthesis Primary synthetic sites are extrahepatic, but liver is key regulator of homeostasis Key concepts: absorption Largest source is biliary secretion, not diet. Normal absorption: 50% For cholesterol to be absorbed it must: undergo hydrolysis (de-esterification by esterases) be incorporated into micelles be taken up by cholesterol transporter be re-esterified and incorporated into chylomicrons NORMAL CHOLESTEROL METABOLISM
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400 mg/day 1,300 mg/day NORMAL CHOLESTEROL ABSORPTION Oil phase
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400 mg/day 1,300 mg/day 17,400 mg/day NORMAL CHOLESTEROL ABSORPTION Plant sterols compete For cholesterol here Oil phase
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STRUCTURE OF PLANT STEROL ESTERS HO Cholesterol Sitosterol HO O C - O Sitosterol Ester
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400 mg/day 1,300 mg/day 17,400 mg/day 850 mg/day NORMAL CHOLESTEROL ABSORPTION Ezetimibe competes For cholesterol here Oil phase
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400 mg/day 1,300 mg/day 17,400 mg/day 850 mg/day NORMAL CHOLESTEROL ABSORPTION Defect in ABCG5/G8 transporter causes phytosterolemia Oil phase
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Role of Bile Salts, cholesterol, phospholipids in gall stone formation. Importance of Bile Salts for cholesterol absorption NORMAL CHOLESTEROL METABOLISM Key concepts: bile salt absorption inhibitors Bile acid binding compounds: Welchol Cholestyramine Colestipol Fiber Surgery: Partial ileal bypass.
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Bile Acid Synthesis HO Cholesterol OH OH OH COOH OH OH COOH OH COOH OH OH COOH Chenodeoxycholic Acid Lithocholic Acid Cholic Acid Deoxycholic Acid
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NORMAL CHOLESTEROL METABOLISM 0.8 G SYN CHOL .65 G .20 G 0.85 G ABS CHOL 50% 0.4 G CHOL 1.3 G CHOL .20 G CHOL 0.65 G CHOL
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17 G BA* NORMAL CHOLESTEROL METABOLISM 0.8 G SYN CHOL 17.35 G BA* 0.85 G ABS CHOL 0.35 G BA* .35 G .65 G .20 G 1.20 G CHOL + BA 50% 95% 0.4 G CHOL 1.3 G CHOL * BA = BILE ACIDS .20 G CHOL 0.65 G CHOL
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Key concepts: absorption Triglyceride (i.e. energy) assimilation is key to the survival of the organism. Dietary triglyceride must be hydrolyzed to fatty acids, mono-glycerides and glycerol prior to absorption. Fatty acids must partition to micellar phase for absorption. For transport, triglyceride must be reconstituted from glycerol and fatty acid and incorporated into chylomicrons. NORMAL TRIGLYCERIDE METABOLISM
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Structures of Fatty Acids C HO O C HO O C HO O C HO O C HO O 18:0 cis-18:1 -6 trans-18:1 -6 18:2 -6 18:3 -3
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Structures of Fatty Acids C HO O C HO O C HO O C HO O C HO O 16:0 (palmitic) cis-18:1 -6 (oleic) trans-18:1 -6 (elaidic) 18:2 -6 (linoleic) 18:3 -3 (alpha linolenic) C HO O 20:5 -3 (EPA)
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FATTY ACIDS (ALBUMIN) TG (VLDL) TG (CHYLO- MICRONS) LIPO- PROTEIN LIPASE Fatty Acid and Triglyceride Flux
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PlasmaTriglyceride (VLDL) Dietary Carbohydrate Increases VLDL Production DietaryCarbohydrate
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Effect of Carbohydrate Restriction on Carbohydrate-induced Hypertriglyceridemia Reisell et al., Am J Clin Nutr 1966;19:84 Treatment: Fast for average 5 days, then consume low CHO diet. Compositionof diet: 7-15% CHO25-30% Prot60-65% Fat
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Lipoprotein Metabolism
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Cholesterol Ester Synthesis HO Cholesterol COOH COO COO OPOO N + Cholesterol Ester COO COO COO OPOO N + Lysolecithin Lecithin-Cholesterol Acyl Transferase (LCAT) Acyl-Cholesterol Acyl Transferase (ACAT)
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Lipoproteins: Separation by – Electrophoresis Density Size by Electron Microscopy
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Pancreatic Lipase Movement Most pancreatic lipase is secreted into the pancreatic duct, but some moves back into capillaries.
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Chylomicron Role in Pancreatitis Pancreatic lipase acts on chylomicrons adherent to capillary endothelium, producing fatty acid anions, or soaps. By detergent action, cell membranes are disrupted, releasing more lipase, and additional fatty acid anions are produced in a vicious cycle.
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Apolipoproteins
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Metabolic RelationshipsAmong Lipoproteins LDL 1. 3. 2. LipoproteinLipase` TG HDL VLDL
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 TRIGLYCERIDES  HDL SMALL DENSE LDL
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Role of CETP in Triglyceride/Cholesteryl Ester Exchange VLDL CETP HDL TG CE LDL CETP HDL TG CE
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Role of Triglycerides in Producing Small Dense LDL or HDL TG TG TG CE CE CE CETP Lipase 1. CE exchanged for TG 2. TG removed
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FREE FATTY ACIDS Dyslipidemia of Metabolic Syndrome VLDL HDL LDL FATTY ACIDSGLYCEROL HDL CATABOLISM UNINHIBITEDLYPOLYSIS
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Distribution of LDL Size Phenotypes According to Triglyceride Levels Phenotype A (light fluffy LDL) Phenotype B (small dense LDL) Cumulative percent of cases Triglyceride (mg/dl) Austin et al, Circulation 1990; 82:495
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Peroxisome Proliferator-Activated Receptor: A Nuclear Receptor for Metabolic Genes a, Basic mechanism of action of nuclear hormone receptors: bind to a specific sequence in the promoter of target genes (called hormone response elements), and activate transcription upon binding of ligand. Several nuclear hormone receptors, including the retinoic acid receptor, the vitamin D receptor and PPAR, can bind to DNA only as a heterodimer with the retinoid X receptor, RXR, as shown. b, some PPAR  and PPAR ligands. Kersten et al. Roles of PPARs in health and disease. Nature 2000; 405: 421-424
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Role of PPAR*  and  in VLDL, LDLand HDL metabolism * Peroxisome Proliferator Activated Receptor PPAR  Tissues: Liver, kidney, heart, muscle. Ligands: fatty acids, fibrates Actions: Stimulate production of apo A I, lipoprotein lipase, increase expression of ABC A-1, increase FFA uptake and catabolism, decrease FFA and VLDL synthesis. PPAR  Tissues: Adipose tissue and intestine. Ligands: arachidonic acid, Glitazones Actions: increase expression of ABC A-1, increase FFA synthesis and uptake by adipocytes, increase insulin sensitivity (?)
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HDL and Reverse Cholesterol Transport
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HDL and Reverse Cholesterol Transport Tangier Disease
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HDL and Reverse Cholesterol Transport
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HDL and Reverse Cholesterol Transport
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HDL and Reverse Cholesterol Transport
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LDL-R HDL and Reverse Cholesterol Transport
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LDL-R 50% of HDL C may Return to the liver On LDL via CETP HDL and Reverse Cholesterol Transport
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An atherogenic lipoproteincontaining apo(a) and apoB. 20-30% of people have levelssuggesting C-V risk. Black subjects have Lp(a)normal range twice as highas white and Asiatic subjects. Apo(a) sequence similar to plasminogen, and Lp(a)interferes with spontaneous thrombolysis. Lp(a) levels highly genetic, resistant to diet and drugtherapy, although niacin may help. “LDL” Apo(a) -S-S- Lipoprotein(a), or Lp(a)
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Summary – Lipid and Lipoprotein Metabolism Cholesterol absorption, synthesis, and disposition Triglyceride/fatty acid transformations and energy metabolism Lipoprotein core and surface components Lipoprotein origins and destinations governed by apo’s Derangement in the metabolic syndrome Reverse cholesterol transport – the dominant direction Lipoprotein(a) Lipoproteins in the arterial wall