Pathophysiology of lipoprotein transport.
A system for classification of genetic and acquired forms of hyperlipidemia in humans based on lipoprotein physiology is described. Most hyperlipidemia can be accounted for by defects in one of four sites of physiologic regulation: (1) triglyceride-rich lipoprotein production, (2) lipoprotein lipase-mediated triglyceride catabolism, (3) remnant lipoprotein catabolism, and (4) extrahepatic cholesterol-rich lipoprotein catabolism.
D001053:Apolipoproteins / Q000378:metabolism; D001161:Arteriosclerosis / Q000503:physiopathology; D001692:Biological Transport; D002914:Chylomicrons / Q000378:metabolism; D006801:Humans; D006937:Hypercholesterolemia / Q000235:genetics; D006949:Hyperlipidemias / Q000145:classification / Q000235:genetics / Q000378:metabolism*; D008071:Lipoprotein Lipase / Q000172:deficiency / Q000378:metabolism; D008074:Lipoproteins / Q000378:metabolism*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008107:Liver Diseases / Q000503:physiopathology; D010641:Phenotype; D014280:Triglycerides / Q000097:blood; D014973:Xanthomatosis / Q000503:physiopathology
D001053:Apolipoproteins; D002914:Chylomicrons; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D008071:Lipoprotein Lipase