Postprandial lipemia and cardiovascular disease

Abstract

Postprandial lipemia, characterized by a rise in triglyceride-rich lipoproteins after eating, is a dynamic, nonsteady-state condition in which humans spend the majority of time. There are several lines of evidence suggesting that postprandial lipemia increases risk of atherogenesis. Clinical data show a correlation between postprandial lipoproteins and the presence/progression of coronary artery disease and carotid intimal thickness. Mechanistic studies demonstrate that triglyceride-rich lipoprotein remnants may have adverse effects on endothelium and can penetrate into the subendothelial space. Exchange of core lipids between postprandial lipoproteins and low-density lipoprotein (LDL)/high-density lipoprotein (HDL) is increased during prolonged lipemia, resulting in small, dense LDL particles and reduced HDL cholesterol levels. Hemostatic variables, including clotting factors, platelet reactivity, and monocyte cytokine expression, may be increased during postprandial lipemia. Collectively, these data suggest that assessment and treatment of atherosclerosis should include parameters related to postprandial lipemia.

Postprandial Lipid Metabolism: The Missing Link Between Life-Style Habits and the Increasing Incidence of Metabolic Diseases in Western Countries?~!2009-09-30~!2010-01-26~!2010-03-30~!

“…Thirty years ago, it was first proposed by Zilversmit [11] that postprandial lipemia may play a role in atherogenesis, and there is now a great deal of evidence from epidemiological, clinical and experimental studies to support the idea that postprandial hyperlipidemia is an important risk factor for atherosclerosis and the progression of cardiovascular disease [12][13][14][15]. Nakajima and colleagues have reported that the majority of sudden cardiac deaths in a Japanese cohort of patients were associated with postprandial hyperlipidemia [16] and that plasma remnant lipoprotein levels were the major pathological factor involved [17].…”

“…Current evidence suggests that postprandial lipoproteins may be involved in promoting atherosclerosis both directly, via an influence on events in the vasculature, and indirectly, by causing a more atherogenic lipoprotein profile when their levels are abnormally raised [12,14,26]. Atherosclerosis is initiated by dysfunction of the vascular endothelium followed by the formation of macrophage foam cells, generated by the scavenging of lipids from plasma lipoproteins.…”

“…Other pro-inflammatory and potentially atherogenic effects of postprandial lipoproteins include activation of leukocytes, promoting adhesion to the endothelium and invasion of the artery wall [12,40]. In addition, postprandial lipemia causes pro-thrombotic effects such as increasing coagulant factor VII [41] and plasminogen activator inhibitor type 1(PAI-1) activity [42] and increasing platelet activity [14,43] and aggregation [44].…”

“…The composition of TRLs is metabolically linked to that of LDL, with plasma TG levels being the main factor influencing LDL particle size [47], and it has been demonstrated that postprandial hyperlipidemia is associated with an increase in the proportion of small, dense LDL [46,[48][49][50]. In addition, prolonged lipemia leads to increased opportunity for the transfer of core lipids between TRLs and high density lipoprotein (HDL), leading to a reduction in HDL cholesterol levels [14]. This combination of high plasma TG concentrations, increased small dense LDL and low HDL is known as the lipid triad or atherogenic lipoprotein profile [51].…”

C-terminal interactions of apolipoprotein E4 respond to the postprandial state

“…triglyceride-rich lipoproteins Chronic vascular inflammation is increasingly recognized as playing a central role in atherosclerosis (1,2). Recent studies have focused on repetitive injury of the vascular wall during the postprandial state (3,4), where endothelial cells lining the vascular wall are repeatedly exposed to a wide variety of lipoproteins, cytokines, and hemostatic, inflammatory, and anti-inflammatory factors. Little is known about how these postprandial factors influence lipid metabolism, and specifically the behavior of apolipoproteins in the preprandial and postprandial state.…”