Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins

Abstract

Patients with coronary artery disease (CAD) often have increased postprandial triglyceride levels compared with healthy control subjects, and it has been demonstrated that plasma triglyceride concentration in the fed state is an independent predictor of CAD. Increased postprandial triglyceridemia is strongly associated with a constellation of potentially atherogenic and thrombogenic lipoprotein changes, including a) increase in the plasma concentration of intestinally derived chylomicrons and their remnants; b) increase in the level of hepatic very low density lipoproteins and their remnants; c) decrease in level of high density lipoprotein (HDL) cholesterol because of increase in cholesteryl transfer from HDL to postprandial triglyceride-rich lipoproteins (TRL); d) decrease in low density lipoprotein (LDL) size, associated with increased susceptibility of LDL to oxidation; and e) increase in the association of lipoprotein (a) with TRL. Postprandial TRL are potentially thrombogenic because they are associated with increased activated factor VII activity (a procoagulant effect) and increased levels of plasminogen activator inhibitor-1 (an antifibrinolytic effect). Experimental results and clinical trial data suggest that plasma accumulation of remnant lipoproteins (in the fed or fasted state) is not just an associated feature of an atherogenic lipoprotein profile but that TRL remnants themselves contribute to the pathogenesis of atherosclerosis. Diet and/or drug treatments that lower the level of TRL in the fasted state also tend to have a beneficial effect on postprandial lipoprotein levels. Thus, aerobic exercise, weight reduction and triglyceride-lowering medications all reduce postprandial triglyceridemia and have the potential to reduce the level of atherogenic remnant lipoproteins.