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.
Highlights
Hyperlipidemia clinical diagnosis requires fasting lipemia, but individuals are in the postprandial state for most of the 24 h
Endothelial function decreased to 3.3 ± 0.5% (p = 0.03) compared with 5.9 ± 1.1% at baseline, and flow-mediated vasodilation (FMD) reduced from baseline level of 5.9 ± 1.1 to 3.3 ± 0.4% (p = 0.04), manifesting that postprandial lipemia leads to endothelial dysfunction by changing circulating blood lipids [46]
These results indicate that high-fat meal (HFM) can promote the apoptosis of endothelial cells, and the apoptosis rate is closely related to the increase in MPO and proMMP-9 activity, suggesting a possible mechanism of endothelial injury induced by postprandial lipemia [74] (Figure 1)
Summary
Hyperlipidemia clinical diagnosis requires fasting lipemia, but individuals are in the postprandial state for most of the 24 h. Postprandial serum TG and PMAactivated leukocyte O−2 production were significantly higher than before meal, whereas the postprandial FMD level was lower than before meal, which suggested that an acute increase in postprandial TG may cause endothelial dysfunction through elevated oxidative stress. FMD in T2D and IGT patients decreased significantly at 4 h, demonstrating that the changes of postprandial lipemia were closely related to the systematic markers of oxidative stress and led to the impairment of vasodilation function [57]. Postprandial serum significantly increased the percentage of annexin-positive HUVECs and the activity of caspase-3 These results indicate that HFM can promote the apoptosis of endothelial cells, and the apoptosis rate is closely related to the increase in MPO and proMMP-9 activity, suggesting a possible mechanism of endothelial injury induced by postprandial lipemia [74] (Figure 1). A study to evaluate the effect of 4 h interrupted sitting with 5 min stair climbing after an HFM on vascular found that FMD decreased from 9.41 ± 2.61 to 10.34 ± 3.30% after exercise, indicating that
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