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Am J Physiol Endocrinol Metab 279: E1039-E1044, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 5, E1039-E1044, November 2000

Lipid oxidation is reduced in obese human skeletal muscle

Jong-Yeon Kim, Robert C. Hickner, Ronald L. Cortright, G. Lynis Dohm, and Joseph A. Houmard

Departments of Biochemistry, Physiology, Exercise, and Sport Science and The Human Performance Laboratory, East Carolina University, Greenville, North Carolina 27858

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 from 14C-labeled fatty acids. Palmitate oxidation, which is at least partially dependent on carnitine palmitoyltransferase-1 (CPT-1) activity, was depressed (P < 0.05) by approx 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 approx 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 (approx 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.

carnitine palmitoyltransferase; fatty acids; malonyl-coenzyme A


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