Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity.

摘要: Abstract Traditional risk factors for coronary artery disease (CAD) predict about 50% of the developing CAD. The Adult Treatment Panel (ATP) III has defined emerging CAD, including small, dense low-density lipoprotein (LDL). Small, LDL is often accompanied by increased triglycerides (TGs) and low high-density (HDL). An number particles missed when cholesterol level normal or borderline elevated. are present in families with premature CAD hyperapobetalipoproteinemia, familial combined hyperlipidemia, subclass pattern B, dyslipidemic hypertension, syndrome X. metabolic syndrome, as ATP III, incorporates a components these syndromes, insulin resistance intra-abdominal fat. Subclinical inflammation elevated procoagulants also appear to be part this atherogenic syndrome. Overproduction very lipoproteins (VLDLs) liver secretion large, apolipoprotein (apo) B-100–containing VLDL primary characteristic most patients. TG hydrolyzed lipase (LPL) which produces intermediate-density lipoprotein. further, resulting generation LDL. esters exchanged ester tranfer proteins, followed hydrolysis hepatic Cholesterol transfer protein mediates similar lipid exchange between HDL, producing ester–poor HDL. In adipocytes, reduced fatty acid trapping retention adipose tissue may result from defect incorporation free acids into TGs. Alternatively, promote adipocytes. Both abnormalities lead levels plasma, flux back liver, enhanced production TGs, decreased proteolysis apo B-100, production. Decreased removal postprandial TGs accompanies abnormalities. Genes regulating expression major players cascade, such LPL, protein, lipase, can modulate but not defects. New candidates gene effects have been identified on chromosome 1. Regardless their fundamental causes, (compared LDL) prolonged residence time more susceptible oxidation because interaction receptor, enter arterial wall easily, where they retained readily. promotes endothelial dysfunction cells. animal models atherosclerosis human epidemiologic studies clinical trials, (particularly numbers) appears than patients HDL hypertriglyceridemia) requires use lipid-altering drugs decrease convert them larger, buoyant next critical step further reduction will correct diagnosis treatment dyslipidemia that it.