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1 Department of Physiology, East Carolina Uninversity, Greenville, NC, USA
2 Department of Exercise and Sport Science, Human Performance Laboratory, East Carolina University, Greenville, NC, USA
3 Department of Physiology, East Carolina Uninversity, Greenville, NC, USA; Department of Exercise and Sport Science, Human Performance Laboratory, East Carolina University, Greenville, NC, USA
4 Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC, USA
5 Department of Surgery, East Carolina University, Greenville, NC, USA
6 Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: hulverm{at}mail.ecu.edu.
The objectives of this study were to: 1) examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity; and 2) determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long chain fatty acyl CoAs. Muscle was obtained from normal weight [N=8; body mass index (BMI), 23.8±0.58 kg/m2], overweight/obese (N=8; BMI, 30.2±0.81 kg/m2), and extremely obese (N=8; BMI, 53.8±3.5 kg/m2) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long chain fatty acyl CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58% and 83% lower in skeletal muscle from extremely obese (44.9±5.2 nmole/g/h) patients compared to normal weight (71.0±5.0 nmole/g/h) and overweight/obese (82.2±8.7 nmole/g/h), respectively. Palmitate oxidation was negatively (R=-.44, P=.003) associated with BMI. Long chain fatty acyl CoA content was higher in both the overweight/obese and extremely obese patients compared to normal weight, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long chain fatty acyl CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity; and that the accumulation of intra-myocellular long chain fatty acyl CoAs are not solely a result of reduced fatty acid oxidation.
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