Abstract
Abnormalities in postprandial lipemia (PPL), particularly those related to triglyceride-rich lipoproteins, are considered an independent cardiovascular risk factor. As diet is known to be one of the main modulators of PPL, the aim of this review was to summarize and discuss current knowledge on the impact of diet and its components on PPL in humans; specifically, the impact of weight loss, different nutrients (quantity and quality of dietary fats, carbohydrates, and proteins), alcohol and other bioactive dietary components (i.e., polyphenols), as well as the effect of different dietary patterns. The possible mechanisms behind the metabolic effects of each dietary component were also discussed.
Highlights
Abnormalities in postprandial lipemia (PPL), those related to triglyceride-rich lipoproteins (TRL), have been considered an independent cardiovascular risk factor, even more important than altered fasting triglyceride (TAG) metabolism [1]
An saturated fatty acid (SFA) meal resulted in a prolonged increase in ApoB100 concentrations that fell below the post-absorptive values 9 h after meal. These findings suggest that a polyunsaturated fatty acid (PUFA)-diet would acutely stimulate the production of lipoproteins of intestinal origin, while the SFA-diet would chronically stimulate the production of lipoproteins of hepatic origin, determining a prolonged postprandial increase in plasma TAG
PPL is a well-known independent cardiovascular risk factor, human intervention studies evaluating the impact of dietary habits on PPL are rather scarce, and some of them contain notable weaknesses to be considered when drawing conclusions
Summary
Abnormalities in postprandial lipemia (PPL), those related to triglyceride-rich lipoproteins (TRL), have been considered an independent cardiovascular risk factor, even more important than altered fasting triglyceride (TAG) metabolism [1]. The stimulation of hepatic lipogenesis and/or the inhibition of lipid oxidation, and consequent increased synthesis and secretion of lipoproteins of hepatic origin, seems to be the main pathway leading to an increase in plasma triglyceride levels after high-carbohydrate diets, especially those rich in starch and simple sugars This has been highlighted by kinetic studies evaluating the relative contribution of VLDL-triglyceride assembly, production, and clearance. Other studies have evaluated the effects of fiber from natural carbohydrate-foods in medium-term experiments (Table 3) In these trials, a daily intake of dietary fiber ranging between 30 and 52 g reduced postprandial TAG response to a test-meal with a composition similar to the diets tested, when compared with a diet low in fiber and with a high glycemic index or a diet rich in monounsaturated fat (MUFA) [49, 50, 58]. These data suggest that the metabolic effects of dietary fibers may be linked to the type (soluble vs. insoluble) and,
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