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.
Highlights
This review focuses on the kinds of diets, food, and food components that affect postprandial inflammation, endothelial function, and oxidative stress, and which are related to cardiometabolic risk, including metabolic syndrome (MS), and cardiovascular diseases (CVD) and type
The postprandial serum glucose peak was higher after rice milk and correlated positively with an increase in malondialdehyde (MDA, a biomarker of oxidative stress mostly related to lipid peroxidation) and a drop in plasma arginine, suggesting that cow’s milk may limit postprandial hyperglycemia, which in turn may decrease lipid peroxidation and enhance nitric oxide (NO) bioavailability [101]
In a validated rat model [70], we showed that rapeseed protein, and the supplementation of milk protein with l-arginine and l-cysteine, prevented postprandial endothelial dysfunction [118]
Summary
This review focuses on the kinds of diets, food, and food components that affect postprandial inflammation, endothelial function, and oxidative stress, and which are related to cardiometabolic risk, including metabolic syndrome (MS), and cardiovascular diseases (CVD) and type. MS is mainly considered as being related to the development of resistance to the action of insulin in different tissues and on different metabolisms [9], linked closely to the onset of systemic low-grade inflammation, which in turn is associated with the development of abdominal fat [10]. Controlled studies in animals have provided further evidence that insulin resistance, systemic and adipose tissue low-grade inflammation, and vascular endothelial dysfunction, as promoted by western diets, are early features of this cardiometabolic risk cluster [15]. Abnormal nitric oxide (NO) production or signaling and endothelial dysfunction, triggered by excessive exposure to high-fat and high-sucrose foods, may be one important mediator of diet-induced insulin resistance and cardiometabolic risk [26,27]. It should be noted that these studies differed markedly in terms of the methods used to study postprandial metabolism [74]
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