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Higher in vivo fatty acid (FA) oxidation rates have been reported in obese individuals compared to lean counterparts; however whether this reflects a shift in substrate-specific oxidative capacity at the level of the skeletal muscle mitochondria has not been examined. The purpose of this study was to test the hypothesis that in situ measures of skeletal muscle mitochondria FA oxidation would be positively associated with total body fat. Participants were 38 premenopausal women (BMI=26.5±4.3 kg/m2). Total and regional fat were assessed by dual-energy X-ray absorptiometry (DXA). Mitochondrial FA oxidation was assessed in permeabilized myofibers using high-resolution respirometry and a palmitoyl carnitine substrate. We found positive associations of total fat mass with State 3 (ADP-stimulated respiration) (r=0.379, p<0.05) and the respiratory control ratio (RCR, measure of mitochondrial coupling) (r=0.348, p<0.05). When participants were dichotomized by high or low body fat percent, participants with high total body fat displayed a higher RCR compared to those with low body fat (p<0.05). There were no associations between any measure of regional fat and mitochondrial FA oxidation independent of total fat mass. In conclusion, greater FA oxidation in obesity may reflect molecular processes that enhance FA oxidation capacity at the mitochondrial level. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Elevated serum high-sensitivity C-reactive protein (hs-CRP) and low serum 25-hydroxyvitamin D [25(OH)D] are associated with increased cardiovascular disease (CVD) risk. Ethnic differences in serum hs-CRP and 25(OH)D concentrations and CVD are known. Objectives: to investigate the ethnic differences in hs-CRP concentrations, to assess the influence of 25(OH)D on these ethnic differences and to examine the influence of 25(OH)D on association between hs-CRP and cardiovascular health indices. Subjects: 62 healthy adults [26 African Americans (AA), 26 European Americans (EA), and 10 Hispanic Americans (HA)], ages 18-55 years. Serum hs-CRP and 25(OH)D as well as pulse wave velocity (PWV), augmentation index (AIx), and flow-mediated dilatation (FMD) were measured. hs-CRP was inversely associated with 25(OH)D (r = -0.25, P = 0.049), and hs-CRP was positively associated with PWV (r = 0.29, P = 0.04). The association of hs-CRP with PWV attenuated after adjustment for 25(OH)D (P = 0.15). hs-CRP was higher in AA compared to EA (P = 0.05); this differences was reduced by 32% after adjusting for serum 25(OH)D. Conclusion: eventhough the inverse association between serum 25(OH)D and CRP does not infer causality, lower serum 25(OH)Dmay increase risk for inflammation and endothelial dysfunction. The lower 25(OH)D in AA may predispose to greater inflammation and associated vascular dysfunction. [ABSTRACT FROM AUTHOR]