Affiliation:
1. Departments of Biochemistry, Physiology, Exercise, and Sport Science and The Human Performance Laboratory, East Carolina University, Greenville, North Carolina 27858
Abstract
The purpose of this study was to discern cellular mechanisms that contribute to the suppression of lipid oxidation in the skeletal muscle of obese individuals. Muscle was obtained from obese [body mass index (BMI), 38.3 ± 3.1 kg/m2] and lean (BMI, 23.8 ± 0.9 kg/m2) women, and fatty acid oxidation was studied by measuring 14CO2 production from14C-labeled fatty acids. Palmitate oxidation, which is at least partially dependent on carnitine palmitoyltransferase-1 (CPT-1) activity, was depressed ( P < 0.05) by ≈50% with obesity (6.8 ± 2.2 vs. 13.7 ± 1.4 nmole CO2 · g−1 · h−1). The CPT-1-independent event of palmitoyl carnitine oxidation was also depressed ( P < 0.01) by ≈45%. There were significant negative relationships ( P < 0.05) for adiposity with palmitate ( r = −0.76) and palmitoyl carnitine ( r = −0.82) oxidation. Muscle CPT-1 and citrate synthase activity, an index of mitochondrial content, were also significantly ( P < 0.05) reduced (≈35%) with obesity. CPT-1 ( r = −0.48) and citrate synthase ( r = −0.65) activities were significantly ( P < 0.05) related to adiposity. These data suggest that lesions at CPT-1 and post-CPT-1 events, such as mitochondrial content, contribute to the reduced reliance on fat oxidation evident in human skeletal muscle with obesity.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism
Cited by
505 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献