The Postprandial Appearance of Features of Cardiometabolic Risk: Acute Induction and Prevention by Nutrients and Other Dietary Substances

Abstract

The purpose of this review is to provide an overview of diets, food, and food components that affect postprandial inflammation, endothelial function, and oxidative stress, which are related to cardiometabolic risk. A high-energy meal, rich in saturated fat and sugars, induces the transient appearance of a series of metabolic, signaling and physiological dysregulations or dysfunctions, including oxidative stress, low-grade inflammation, and endothelial dysfunction, which are directly related to the amplitude of postprandial plasma triglycerides and glucose. Low-grade inflammation and endothelial dysfunction are also known to cluster together with insulin resistance, a third risk factor for cardiovascular diseases (CVD) and type-II diabetes, thus making a considerable contribution to cardiometabolic risk. Because of the marked relevance of the postprandial model to nutritional pathophysiology, many studies have investigated whether adding various nutrients and other substances to such a challenge meal might mitigate the onset of these adverse effects. Some foods (e.g., nuts, berries, and citrus), nutrients (e.g., l-arginine), and other substances (various polyphenols) have been widely studied. Reports of favorable effects in the postprandial state have concerned plasma markers for systemic or vascular pro-inflammatory conditions, the activation of inflammatory pathways in plasma monocytes, vascular endothelial function (mostly assessed using physiological criteria), and postprandial oxidative stress. Although the literature is fragmented, this topic warrants further study using multiple endpoints and markers to investigate whether the interesting candidates identified might prevent or limit the postprandial appearance of critical features of cardiometabolic risk.

Effects of tree nut and groundnut consumption compared with those of l-arginine supplementation on fasting and postprandial flow-mediated vasodilation: Meta-analysis of human randomized controlled trials

“…Moreover, differences could have been caused by different effects on inflammation. However, two meta-analyses showed that longer-term consumption of tree nuts [57] and L-arginine supplementation [58] did not affect fasting inflammation, whereas positive effects of tree nut consumption on postprandial markers of inflammation and oxidative stress has been reported [59]. However, L-arginine supplementation did not affect postprandial inflammation [35], which might be due to the short half-life of L-arginine of about 90 min [60].…”

Effects of Acute Cocoa Supplementation on Postprandial Apolipoproteins, Lipoprotein Subclasses, and Inflammatory Biomarkers in Adults with Type 2 Diabetes after a High-Fat Meal

“…Postprandial hyperglycemia and hyperlipidemia exacerbate postprandial systemic inflammation and vasoconstriction. The degree of response can be assessed by measuring select inflammatory biomarkers and nitrite that are sensitive to dietary challenges [ 55 ]. In randomized controlled clinical trials, acute interventions with dietary polyphenols have shown promise in mitigating postprandial inflammation.…”

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

“…The release of fatty acids from solid food was lower than that from liquid or semisolid food, and the postprandial TG elevation caused by solid food was lower than that of liquid food ( 101 ). A range of metabolic, physiological, or functional disorders may occur transiently after ingestion of a high-energy diet rich in fat, and the process is strongly associated with postprandial TG ( 102 ). Postprandial CM-TG response increased with an increase in dietary fat content in normal weight and obese individuals ( 79 ).…”