HDLs and alimentary lipemia. Studies in men with previous myocardial infarction at a young age.

Abstract

The plasma concentration, particle size, and chemical composition of high density lipoproteins (HDLs) are associated with the metabolism of triglyceride-rich lipoproteins (TGRLs). During alimentary lipemia there is active exchange of lipids and apolipoproteins between HDL and apolipoprotein B-containing lipoproteins. Whereas HDL has been assigned a protective role against the development of atherosclerosis, alimentary lipemia has been proposed to represent a potentially atherogenic state. We examined plasma HDL concentration, particle size, and composition and their relations to postprandial TGRLs in 32 postinfarction patients and 10 healthy control subjects after intake of a standardized oral fat load of a mixed-meal type. All patients had undergone coronary angiographies in connection with the myocardial infarction and around 5 years thereafter. The plasma HDL cholesterol concentration decreased significantly in response to the oral fat load, particularly in hypertriglyceridemic patients, with a concomitant increase of HDL triglycerides. A limited and reversible yet consistent increase of HDL particle size (1-2%) was seen 6 hours after intake of the oral fat load on nondenaturing gradient gel electrophoresis (GGE) in both patients and control subjects. shown an independent inverse relation between the high density lipoprotein (HDL) cholesterol concentration and the risk of future coronary heart disease (CHD).1 The mechanisms underlying this negative association as well as the seemingly protective effect of HDL against the development of coronary atherosclerosis are not well defined. It has been hypothesized either that HDL exerts a direct protective effect by facilitating cholesterol transport from peripheral tissues, including the arterial wall, 2 -3 or that a low plasma HDL level merely reflects metabolic processes that are associated with the development of atherosclerosis. 4 The processes involved in the delivery of choFrom the

Triglyceride‐rich lipoproteins in non‐insulin‐dependent diabetes mellitus: post‐prandial metabolism and relation to premature atherosclerosis

“…Several studies support the concept that an exaggerated alimentary lipaemia predisposes to coronary artery disease (CAD) [98,[131][132][133][134][135][136][137][138][139][140]. Karpe et al [98] compared post-prandial lipoprotein metabolism in healthy subjects and patients with CAD, and demonstrated an impaired post-prandial lipoprotein metabolism in the patient group. Moreover, experimental and clinical studies have demonstrated that TRL remnants are atherogenic [133][134][135][136][137][138][139][140].…”

Postprandial lipoprotein metabolism and atherosclerosis

“…Several reports testify that the transfer of cholesteryl esters from HDL to the TRL fraction is enhanced during alimentary lipaemia [65±69]. As a result HDL is depleted of cholesterol, whereas the HDL particle concentration measured as apo A-I containing lipoprotein particles with and without apo A-II is unaffected by oral fat intake [70]. Theoretically, the transfer of cholesterol from HDL into the TRL pool may be regulated on two levels, first by the concentration of CETP, and secondly by the abundance of acceptor lipoproteins, which increases in the postprandial state, partly as a result of the delayed rate of TRL clearance.…”

Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM

“…[Diabetologia (1994) proteins of intestinal origin were higher in patients with NIDDM [2]. In 1979 Zilversmit [3] suggested that triglyceride-rich lipoproteins of intestinal origin, especially the cholesteryl ester-rich chylomicron remnants, could play a very important role in atherogenesis, and since then, several reports have been published supporting this hypothesis [4][5][6][7][8][9][10]. Thus, our observation that postprandial lipaemia was increased in NIDDM raised the possibility that abnormalities in the metabolism of intestinally-derived lipoproteins may contribute to the increased risk of CHD in these patients.…”