Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

Abstract

Postprandial lipemia plays an important role in the formation, occurrence, and development of atherosclerosis, and it is closely related to coronary heart disease and other diseases involving endothelial dysfunction, oxidative stress, inflammation, and other mechanisms. Therefore, it has become a focus area for further research. The studies on postprandial lipemia mainly include TG, TRL, VLDL, CM, and remnant cholesterol. Diurnal triglyceride patterns and postprandial hyperlipidemia are very relevant and are now insufficiently covered. The possible mechanisms between postprandial lipemia and cardiovascular disease have been reviewed in this article by referring to relevant literature in recent years. The research progress on the effects of postprandial lipemia on endothelial function, oxidative stress, and inflammation is highlighted. The intervention of postprandial lipemia is discussed. Non-medicinal intervention such as diet and exercise improves postprandial lipemia. As medicinal intervention, statin, fibrate, ezetimibe, omega-3 fatty acids, and niacin have been found to improve postprandial lipid levels. Novel medications such as pemafibrate, PCSK9, and apoCIII inhibitors have been the focus of research in recent years. Gut microbiota is closely related to lipid metabolism, and some studies have indicated that intestinal microorganisms may affect lipid metabolism as environmental factors. Whether intervention of gut microbiota can reduce postprandial lipemia, and therefore against AS, may be worthy of further study.

A Gene Variation at the ZPR1 Locus (rs964184) Interacts With the Type of Diet to Modulate Postprandial Triglycerides in Patients With Coronary Artery Disease: From the Coronary Diet Intervention With Olive Oil and Cardiovascular Prevention Study

“…Thus, postprandial triglyceride levels independently predict the risk of coronary artery disease (CAD), peripheral vascular disease, and cerebrovascular disease and may be stronger predictors of cardiovascular disease (CVD) than fasting triglycerides (6)(7)(8)(9)(10). This may be due to the proinflammatory, procoagulant, and prooxidant environment that characterizes the physiological response to dietary intakes, particularly a high-fat meal (11,12). Specifically, the main mechanisms proposed for atherosclerosis induced by postprandial lipemia include: (1) endothelial dysfunction induced by increased plasma TG with decreased serum nitrite/nitrate levels and flow-mediated dilation, (2) an increase in reactive oxygen species mediated through mitochondrial dissociation and beta-oxidation, (3) increased expression of adhesion factors at the subendothelial level, (4) activation of complement component factor 3, and (5) upregulation of proinflammatory and pro-apoptotic genes in endothelial cells following fat intake (12)(13)(14)(15).…”

Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis

“…The clinical significance of the TGRL remnants has been mostly assigned to their ability to enter the arterial intima and to contribute to the formation of foam cells. However, the mechanisms by which postprandial lipemia induces atherosclerosis also involve induction of endothelial dysfunction, oxidative stress, and inflammation ( 315 ). Importantly, the lipoprotein lipase -mediated hydrolytic modification of the TGRLs takes place not only in capillaries but also in atherosclerosis-susceptible arterial segments where it results in high local concentrations of lipolytic products, such as oxidized free fatty acids which jointly with the TGRLs cause a multitude of inflammatory reactions in the ECs and the cells within the intima ( 316 , 317 ).…”

Effects of Postprandial Lipemia Combined With Disturbed Blood Flow on the Flow-Mediated Dilation, Oxidative Stress, and Endothelial Microvesicles in Healthy Subjects

“…An important risk factor for endothelial dysfunction is postprandial lipidemia (PPL) ( Nordestgaard et al, 2007 ; Nakamura et al, 2016 ; Zhao et al, 2021 ). The ingestion of a high-fat meal increases serum triglyceride concentrations, induces systemic oxidative stress, and impairs flow-mediated dilation (FMD) in both healthy subjects and patients with dyslipidemia ( Tsai et al, 2004 ; Cortés et al, 2006 ; Ramírez-Vélez, 2011 ; Petersen et al, 2020 ).…”

“…The ingestion of a high-fat meal increases serum triglyceride concentrations, induces systemic oxidative stress, and impairs flow-mediated dilation (FMD) in both healthy subjects and patients with dyslipidemia ( Tsai et al, 2004 ; Cortés et al, 2006 ; Ramírez-Vélez, 2011 ; Petersen et al, 2020 ). Postprandial lipidemia-induced vascular endothelial dysfunction is thought to be mediated by oxidative stress resulting from an increased lipid load within the cell, in turn leading to increased oxidative metabolism and excess production of reactive oxygen species (ROS) ( Ramírez-Vélez, 2011 ; Zhao et al, 2021 ).…”