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LIPOPROTEIN METABOLISM

Home > Study Notes > LIPOPROTEIN METABOLISM
Published in: Biology
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A concise note on lipoprotein metabolism, hope it can be beneficial.

Nik N / Kota Bahru

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Qualification: Bachelor in Medicine and Surgery

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  1. LIPOPROTEIN METABOLISM 1.How lipid is found in the body? 2.What are the lipids in our plasma/serum? 3. How lipid is transferred in body fluid? 4. What is lipoprotein 5. What is the function of li o rotein? 6. What are the characteristics of lipoprotein? 7. Classify the lipoprotein 8. General structure of lipoprotein • membrane-associated lipids • droplets of TG in adipocytes (stored) • Serum/plasma lipids 1. Triglycerides 2. Cholesterol & Cholesterol Ester 3. Free Fatty Acids 4. Phospholipids FFA — by binding to albumin carrier Others — through lipoprotein A macromolecule complex with lipid and specific protein - to transport lipid in plasma (exogenous and endogenous) - dynamic - can interchange lipid and apo's with each other Lipoprotein Chylomicrons Very Low Density Lipid (VLDL) Intermediate-density lipoprotein (IDL) Low-density lipoprotein (LDL) High-density lipoprotein (HDL) Lipoprotein Structure
  2. EXOGENOUS LIPID PATHWAY Chylomicron synthesized in the intestine (Packed with TG, Chol, PL, apo 848) Release to the blood Pick up apo Cll and apo E from circulating HDL called nascent chylomicron Recognized by Lipoprotein Lipase (LPL) Activated by apo- (Triglycerides cleaved Free Fatty Acids Glycerol Func : transport dieterv lipid Intestine Blood Vessel Store by adipose tissue Used by muscle (enerev ) Metabolized by liver (gluconeogenesis, elvcolvsis. lioid svnthesis After TG catabolize , the CM decreased in size (Apo C return to HDL) and called CM remnant Taken up by the liver Recognized by apo E Catabolized and recycle Clinical siqnificance 1 .Deficiency of apo Cll / LPL - accumulation of CM in blood. - type 1 hyperlipoproteinemia (chylomicronemia) 2. Apo E deficiency — CM remnant accumulation - Familial type Ill hyperlipoproteinemia.
  3. Function: transport lipid synthesized in liver to the peripheral tissue ENDOGENOUS PATHWAY VLDL synthesized in liver (packed with Apo B-lOO, TG, Cholesterol) Leave to blood vessel and receive Apo-C11 and Apo E from circulating HDL Recognized by Lipoprotein Lipase (LPL) — activate by Apo C-11 TG broken down into FFA and glycerol VLDL VLDL remnant (IDL) (IDL) IDL formed after TG is broken down VLDL undergo 4eJjpj4atign Low Density Lipoprotein (LDL) - taken up by liver - by LDL receptor which recognized Apo E Intermediate Density Lipoprotein -VLDL return Apo E and Apo C-11 to the HDL / Apo BIOO remained. - TG is also transferred to HDL by CETP (cholesterol ester transfer Low Density Lipoprotein (LDL) -taken up by liver or peripheral tissue by LDL receptor - LDL receptor recognized Apo BIOO
  4. Cellu(QV cholesænl Cho\cs+eot t HM&Coh Y@dqctqo ihhbrted - reduce de novo Sbn-frøqs Now LOU receptor V LOC receptor gznvV I-omit—of LDC entry lhfo ceil RChT (lhusd Cholcså-e€0J CE
  5. REVERSED CHOLESTEROL TRANSPORT (HDL METABOLISM) HDL = supply apo Cll E to CM and VLDL = Transport cholesterol from peripheral tissue to liver Nascent HDL (contain and PL) Circulate in blood, taking unesterified cholesterol from other lipoprotein/cell membrane/macrophage (PL in HDL are solubilizers) Convert free cholesterol to cholesterol ester with enzyme Lecithin Cholesterol Acyl Transferase (LCAT) Receive more ree cholesterol CE converted taken up by liver -Direct uptake -Transferring CE to the TG-rich lipoproteins (chylomicrons and VLDL) with the help of cholesterol ester transfer protein (CETP) in exchange for triglyceride Hyperlipidemia Clinical Siqnificances —Elevation of lipid in plasma (abnormal lipoprotein metabolism) —Atherosclerosis — lead to coronary artery disease (CAD) _ result of partial or total blockade of coronary arteries due to formation of atheroma plaque (atherosclerosis) - Cause bytTC, TLDL-C,JHDL
  6. Receptoy mediated endoqfroms fuse w/ endosemo BOSOSOVhe- anot-adL LOL Comp oncnf amthD o.CAd (independent risk factor for coronary heart disease (CHD)) fro m Etcpwr

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