Lipoprotein Metabolism
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51 Terms
Q: Why are lipoproteins necessary?
A: TG and cholesterol are hydrophobic and cannot travel freely in aqueous blood.
Q: What is the basic structure of a lipoprotein?
A: Hydrophobic core of TG + cholesteryl esters surrounded by phospholipids, free cholesterol, and apoproteins.
Q: How does lipid/protein content affect lipoprotein density?
A: More TG → lower density; more protein → higher density.
Q: What is the density order of lipoproteins?
A: Chylomicron → VLDL → IDL → LDL → HDL.
Q: What are the three major lipoprotein pathways?
A: Exogenous: diet → chylomicron → remnant → liver; endogenous: liver → VLDL → IDL → LDL; reverse cholesterol transport: tissues → HDL → liver.
Q: What is ApoB-48 and where is it made?
A: Structural protein of chylomicrons, made in the intestine by RNA editing of ApoB mRNA.
Q: What is ApoB-100 and what does it do?
A: Structural protein of VLDL/IDL/LDL and ligand for the LDL receptor.
Q: What do ApoC-II and ApoE do?
A: ApoC-II activates LPL; ApoE mediates hepatic uptake of remnants.
Q: What does ApoA-I do?
A: Major HDL apoprotein that activates LCAT.
Q: What is the easiest Apo memory?
A: B-48 = chylomicron; B-100 = VLDL/IDL/LDL + LDLR; C-II = LPL; E = remnants; A-I = LCAT.
Q: How are chylomicrons assembled?
A: Intestinal ApoB-48 + lipids + MTP → nascent chylomicron.
Q: What does MTP do, and what disease results from its deficiency?
A: Loads lipids onto ApoB; deficiency causes abetalipoproteinemia.
Q: How do chylomicrons reach the bloodstream?
A: Intestinal lymphatics → thoracic duct → blood.
Q: What happens when chylomicrons mature?
A: They receive ApoC-II and ApoE from HDL.
Q: What does LPL do to chylomicrons?
A: ApoC-II activates LPL, which hydrolyzes TG → fatty acids + glycerol.
Q: What happens to the fatty acids released by LPL?
A: Muscle can use them for energy; adipose can store them as TG.
Q: What happens to a chylomicron after most TG is removed?
A: It becomes a chylomicron remnant, retains ApoE, and is taken up by the liver.
Q: What is the key difference between ApoC-II and ApoE in chylomicron metabolism?
A: ApoC-II removes TG via LPL; ApoE gets the remnant into the liver.
Q: What causes fat malabsorption?
A: Pancreatic insufficiency, decreased bile salts/obstruction, or intestinal disease.
Q: What does colipase do?
A: Anchors pancreatic lipase to the lipid-water interface so lipase can function despite bile salts.
Q: What are the major consequences of fat malabsorption?
A: Steatorrhea + deficiency of vitamins A, D, E, K.
Q: How is VLDL assembled?
A: Liver ApoB-100 + lipids + MTP → nascent VLDL.
Q: What happens to VLDL in peripheral tissues?
A: ApoC-II activates LPL, which removes TG; VLDL becomes IDL.
Q: What are the two fates of IDL?
A: ApoE-mediated hepatic uptake OR further TG removal → LDL.
Q: What is LDL's main function?
A: Deliver cholesterol to peripheral tissues and liver
Q: How does LDL enter cells?
A: ApoB-100 binds LDLR → receptor-mediated endocytosis → lysosomal processing → cholesterol release.
Q: What happens to the LDL receptor after LDL uptake?
A: It can recycle back to the cell surface.
Q: What does ACAT do?
A: Converts intracellular free cholesterol into cholesteryl ester for storage.
Q: How does high intracellular cholesterol affect LDL receptor synthesis?
A: ↑ cholesterol → ↓ SREBP activity → ↓ LDLR synthesis → ↓ cholesterol uptake.
Q: How does LDL promote atherosclerosis?
A: LDL enters arterial wall → becomes modified/oxidized → macrophage uptake → foam cells → plaque.
Q: Where is HDL produced?
A: Mainly liver and intestine.
Q: What does ABCA1 do?
A: Transfers cellular cholesterol onto nascent HDL.
Q: What disease results from ABCA1 deficiency?
A: Tangier disease → very low HDL.
Q: What activates LCAT?
A: ApoA-I.
Q: What does LCAT do?
A: Esterifies free cholesterol on HDL, producing cholesteryl ester that moves into the HDL core.
Q: What is CETP's function?
A: Exchanges HDL cholesteryl ester for TG from VLDL/ApoB-containing particles.
Q: What receptor allows HDL to deliver cholesterol to the liver?
A: SR-B1.
Q: How is SR-B1 different from LDLR?
A: LDLR → endocytosis of LDL; SR-B1 → selective lipid transfer from HDL without HDL endocytosis.
Q: What is the basic reverse cholesterol transport pathway?
A: Peripheral cholesterol → ABCA1 → HDL → ApoA-I/LCAT → cholesteryl ester → SR-B1 → liver.
Q: What causes Niemann-Pick type C?
A: Defective intracellular cholesterol trafficking, causing lysosomal cholesterol accumulation and prominent neurologic disease.
Q: What is Lp(a)?
A: An LDL-like particle containing ApoB-100 covalently linked to Apo(a).
Q: What does Apo(a) resemble?
A: Plasminogen.
Q: What is the clinical significance of high Lp(a)?
A: It is associated with increased cardiovascular risk, and levels are strongly genetically determined.
Q: Which lipoprotein is largest and least dense?
A: Chylomicron.
Q: Which lipoprotein is smallest and most dense?
A: HDL.
Q: Which lipoprotein primarily carries dietary TG?
A: Chylomicrons.
Q: Which lipoprotein carries liver-derived TG?
A: VLDL.
Q: Which lipoprotein is primarily responsible for cholesterol delivery to tissues?
A: LDL.
Q: Which lipoprotein participates in reverse cholesterol transport?
A: HDL.
Q: Match the key proteins/enzyme functions: LPL, MTP, LDLR, ABCA1, LCAT, CETP, ACAT, SR-B1.
A: LPL: TG hydrolysis; MTP: lipid loading onto ApoB; LDLR: LDL endocytosis; ABCA1: cellular cholesterol → HDL; LCAT: cholesterol esterification on HDL; CETP: CE/TG exchange; ACAT: intracellular cholesterol esterification; SR-B1: HDL cholesterol transfer to liver.
🔥 12 CARDS TO KNOW COLD
B-48 = chylomicrons
B-100 = VLDL → IDL → LDL + LDL receptor binding
C-II = activates LPL
E = remnant uptake by liver
A-I = activates LCAT
MTP = loads lipid onto ApoB
LPL = removes TG from chylomicrons/VLDL
ABCA1 = cellular cholesterol → HDL
LCAT = free cholesterol → cholesteryl ester
CETP = exchanges HDL CE ↔ VLDL TG
LDLR = LDL endocytosis; SR-B1 = selective HDL cholesterol transfer
Chylomicron = dietary TG; VLDL = liver TG; LDL = cholesterol delivery; HDL = reverse cholesterol transport