lipoprotein
Summary
Lipoproteins are spherical particles composed of a hydrophobic core (triglycerides and cholesterol esters) surrounded by a hydrophilic shell (phospholipids, free cholesterol, and apolipoproteins). They transport lipids through the bloodstream and lymphatic system since lipids are insoluble in plasma. Major classes include chylomicrons, VLDL, IDL, LDL, and HDL, each differing in density, size, and apolipoprotein composition, which determines their metabolic fate.
Detail
Lipoproteins solve the problem of transporting hydrophobic lipids (triglycerides, cholesterol) through aqueous plasma. Structure: core of triglycerides/cholesteryl esters surrounded by a monolayer of phospholipids, free cholesterol, and apolipoproteins.
Key classes (in order of decreasing size/increasing density): - Chylomicrons: transport dietary (exogenous) triglycerides from intestine to peripheral tissues; contain ApoB-48, ApoC-II (activates lipoprotein lipase), ApoE. Remnants cleared by liver via ApoE receptor. - VLDL: made by liver, transports endogenous triglycerides; contains ApoB-100, ApoC-II, ApoE. - IDL: intermediate degradation product of VLDL after lipoprotein lipase action. - LDL: 'bad cholesterol'; delivers cholesterol to peripheral tissues; contains ApoB-100; taken up via LDL receptor (mutated/deficient in familial hypercholesterolemia). Elevated LDL is atherogenic, oxidized LDL is taken up by macrophages forming foam cells in atherosclerosis. - HDL: 'good cholesterol'; mediates reverse cholesterol transport from peripheral tissues to liver; contains ApoA-I (activates LCAT). Higher HDL is cardioprotective.
Key enzymes/proteins: Lipoprotein lipase (LPL, endothelial, hydrolyzes triglycerides in chylomicrons/VLDL), Hepatic lipase, LCAT (esterifies cholesterol in HDL), CETP (transfers cholesteryl esters between HDL and VLDL/LDL), PCSK9 (degrades LDL receptor, target of new cholesterol drugs).
Clinical significance: Dyslipidemias are classified by Fredrickson classification based on which lipoprotein is elevated. Familial hypercholesterolemia (LDL receptor defect) causes very high LDL, atherosclerosis, xanthomas. Familial dysbetalipoproteinemia (ApoE2/E2) causes elevated IDL. LPL or ApoC-II deficiency causes hypertriglyceridemia and eruptive xanthomas, pancreatitis. Statins inhibit HMG-CoA reductase, upregulating LDL receptors. PCSK9 inhibitors prevent LDL receptor degradation, lowering LDL further.
Sources
- First Aid for the USMLE Step 1
- Harrison's Principles of Internal Medicine
- Lippincott Biochemistry
- Kaplan USMLE Step 1 Biochemistry
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