Postprandial Hyperlipidemia and Remnant Lipoproteins

Abstract

Fasting hypertriglyceridemia is positively associated with the morbidity of coronary heart disease (CHD), and postprandial (non-fasting) hypertriglyceridemia is also correlated with the risk status for CHD, which is related to the increase in chylomicron (CM) remnant lipoproteins produced from the intestine. CM remnant particles, as well as oxidized low density lipoprotein (LDL) or very low density lipoprotein (VLDL) remnants, are highly atherogenic and act by enhancing systemic inflammation, platelet activation, coagulation, thrombus formation, and macrophage foam cell formation. The cholesterol levels of remnant lipoproteins significantly correlate with small, dense LDL; impaired glucose tolerance (IGT) and CHD prevalence. We have developed an assay of apolipoprotein (apo)B-48 levels to evaluate the accumulation of CM remnants. Fasting apoB-48 levels correlate with the morbidity of postprandial hypertriglyceridemia, obesity, type III hyperlipoproteinemia, the metabolic syndrome, hypothyroidism, chronic kidney disease, and IGT. Fasting apoB-48 levels also correlate with carotid intima-media thickening and CHD prevalence, and a high apoB-48 level is a significant predictor of CHD risk, independent of the fasting TG level. Diet interventions, such as dietary fibers, polyphenols, medium-chain fatty acids, diacylglycerol, and long-chain n-3 polyunsaturated fatty acids (PUFA), ameliorate postprandial hypertriglyceridemia, moreover, drugs for dyslipidemia (n-3 PUFA, statins, fibrates or ezetimibe) and diabetes concerning incretins (dipeptidyl-peptidase IV inhibitor or glucagon like peptide-1 analogue) may improve postprandial hypertriglyceridemia. Since the accumulation of CM remnants correlates to impaired lipid and glucose metabolism and atherosclerotic cardiovascular events, further studies are required to investigate the characteristics, physiological activities, and functions of CM remnants for the development of new interventions to reduce atherogenicity.

Fig. 1.

Chylomicron remnants are accumulated in many metabolic disorders and contributes to the progression of atherosclerotic plaque Many metabolic disorders that correlate the hypertriglyceridemia, postprandial hypertriglyceridemia, type III hyperlipidemia, the metabolic syndrome, diabetes mellitus, impaired glucose tolerance, chronic kidney disease, are related to the accumulation of chylomicron remnants and high apolipoprotein(apo)B-48 concentrations. Chylomicron remnants in sera can directly penetrate into the arterial wall and infiltrate the sub-endothelial space. They enhance systemic inflammation, induce platelet activation, the proliferation of smooth muscle cells, the adhesion of the monocyte, apoptosis of endothelial cells and macrophage foam cell formation. These changes induce the instability and progression of atherosclerotic plaque. High apoB-48 concentrations correlate with the thickening of carotid arteries and the prevalence of coronary artery stenosis.