Abstract
Postprandial hyperlipemia produces long-term derangements in lipid/lipoprotein metabolism, vascular endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity which are strongly linked to atherogenesis. The purpose of this review is to (1) provide a qualitative analysis of the available literature examining the dysregulation of postprandial lipid metabolism in the presence of obesity, (2) inspect the role of adiposity distribution and sex on postprandial lipid metabolism, and (3) examine the role of energy deficit (exercise- and/or energy restriction-mediated), isoenergetic low-carbohydrate diets, and omega-3 (n-3) fatty acid supplementation on postprandial lipid metabolism. We conclude from the literature that central adiposity primarily accounts for sex-related differences in postprandial lipemia and that aerobic exercise attenuates this response in obese or lean men and women to a similar extent through potentially unique mechanisms. In contrast, energy restriction produces only mild reductions in postprandial lipemia suggesting that exercise may be superior to energy restriction alone as a strategy for lowering postprandial lipemia. However, isoenergetic very low-carbohydrate diets and n-3 fatty acid supplementation reduce postprandial lipemia indicating that macronutrient manipulations reduce postprandial lipemia in the absence of energy restriction. Therefore, interactions between exercise/energy restriction and alterations in macronutrient content remain top priorities for the field to identify optimal behavioral treatments to reduce postprandial lipemia.
Highlights
Reductions in vocational physical activity and the availability and consumption of energy-dense foods are often cited as primary culprits of the rising incidence of obesity observed throughout the world [1,2,3,4,5,6]
TRLs (very low-density lipoprotein (VLDL) and chylomicrons (CM)) reduce cholesterol content of high-density lipoproteins (HDL) and decrease the size of low-density lipoproteins (LDL) which increase the propensity for vascular endothelial infiltration and oxidation [8]
Fasting HDL-C concentrations often account for a greater amount of variance in the risk of cardiovascular disease (CVD) compared to TGs leading to their dismissal as a primary risk factor for atherosclerosis [9,10,11]
Summary
Reductions in vocational physical activity and the availability and consumption of energy-dense foods are often cited as primary culprits of the rising incidence of obesity observed throughout the world [1,2,3,4,5,6]. While the contribution of fasting TGs and HDL-C to the overall risk of CVD remains controversial [12, 13], accumulating evidence suggests that exaggerated postprandial lipemia produces rapid derangements of lipid/lipoprotein metabolism, vascular endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity that is strongly linked to atherogenesis [10, 14,15,16,17,18,19,20]. The relationship between postprandial lipid metabolism and atherosclerosis is not surprising when one considers that the majority of individuals following a typical Western Diet consume 3 to 5 meals per day. Interventions which improve the capacity to regulate tissue and blood lipid metabolism following a meal would be expected to lower CVD risk. The purpose of the current review is to (1) provide a qualitative analysis of the available literature examining the dysregulation of postprandial lipid metabolism in the presence of obesity, (2) inspect the role of adiposity distribution and sex on postprandial lipid metabolism, and (3) examine the role and mechanisms by which energy deficit produced via exercise and/or energy restriction, isoenergetic low-carbohydrate diets, and n-3 fatty acid supplementation improves postprandial lipid metabolism
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