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This set covers the vocabulary and core concepts of lipoprotein classifications, structural components, metabolic pathways, and associated clinical disorders from the lecture notes.
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Lipoproteins
Spherical complexes of lipids and specific proteins (apolipoproteins) that transport insoluble lipids, such as triglycerides and cholesterol, through the blood.
Amphipathic Lipids
Lipids such as phospholipids and free cholesterol that surround the hydrophobic interior of a lipoprotein particle.
ApoA-I
The major apolipoprotein of HDL, synthesized in the liver and intestine, which serves as a structural protein and activates the enzyme LCAT.
ApoB-48
A structural protein synthesized in the intestine that is unique to chylomicrons and produced via the RNA editing of the apo B gene.
ApoB-100
A 550,000 Da protein synthesized in the liver that serves as a structural component for VLDL, IDL, and LDL, and acts as a ligand for the LDL receptor.
ApoC-II
An apolipoprotein produced in the liver that acts as a necessary cofactor for the activation of lipoprotein lipase (LPL).
ApoE
An arginine-rich apolipoprotein that acts as a ligand for hepatic uptake of chylomicron remnants and IDL via the LDL receptor.
Chylomicrons (CM)
Large lipoproteins formed in intestinal mucosal cells that are rich in triglycerides (88−99%) and responsible for transporting dietary lipids from the gut to circulation.
Very Low-Density Lipoproteins (VLDL)
Lipoproteins synthesized in the liver to transport endogenously synthesized triglycerides to peripheral tissues.
Low-Density Lipoproteins (LDL)
Cholesterol-rich lipoproteins (48−50% cholesterol) synthesized from VLDL in circulation that transport cholesterol to peripheral tissues.
High-Density Lipoproteins (HDL)
Lipoproteins synthesized in the liver and intestine that transport excess cholesterol from peripheral tissues back to the liver for excretion.
RNA Editing
A process where cytidine deaminase converts a CAA codon to a UAA termination signal in the intestine, resulting in the production of the shorter apoB48 protein instead of apoB100.
Lipoprotein Lipase (LPL)
An enzyme located on the endothelium of extrahepatic tissues that hydrolyzes triglycerides in chylomicrons and VLDL into free fatty acids and glycerol.
LCAT (Lecithin-Cholesterol Acyltransferase)
An enzyme activated by ApoA-I that converts free cholesterol and lecithin on the surface of HDL into cholesteryl esters and lysolecithin.
Reverse Cholesterol Transport
A mechanism by which HDL prevents accumulation of cholesterol in peripheral tissues by transporting it back to the liver for excretion via bile.
Intermediate-Density Lipoprotein (IDL)
Also known as VLDL remnants, these are formed after LPL removes approximately 90% of the triacylglycerol from VLDL.
Familial Hypercholesterolemia
A genetic disorder caused by a defect on chromosome 19 that results in defective LDL receptors, leading to high plasma concentrations of LDL cholesterol and coronary atherosclerosis.
Fatty Liver
An abnormal accumulation of triglycerides inside liver cells caused by impaired VLDL formation or secretion, or by increased synthesis of triglycerides.
Lipotropic Agents
Substances such as choline, methionine, and essential fatty acids that assist in the removal of fats from liver cells and prevent fatty liver formation.
Lipoprotein (a) [Lp(a)]
Known as the 'little rascal,' this highly atherogenic particle is attached to apo B-100 by a disulfide bond and competes with plasminogen to impair fibrinolysis.
Abetalipoproteinemia
An autosomal recessive genetic defect in the synthesis of apo B that results in the total absence of LDL, chylomicrons, and VLDL in circulation, causing fat malabsorption.
Tangier Disease
Also called familial alpha-lipoprotein deficiency, it is caused by an inability to synthesize apo A, leading to nearly absent HDL and the accumulation of cholesteryl esters in tissues.
Normal Plasma Lipid Profile
Clinical values including Total Cholesterol (140−200mg/dl), HDL (40−60mg/dl), LDL (80−130mg/dl), and Triglycerides (50−150mg/dl).