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Am J Physiol Endocrinol Metab (February 20, 2007). doi:10.1152/ajpendo.00639.2006
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Submitted on November 22, 2006
Accepted on February 4, 2007

Skeletal muscle mitochondrial FAT/CD36 and palmitate oxidation are not decreased in obese women

Graham Paul Holloway1*, A. Brianne Thrush2, George J. F. Heigenhauser3, Narendra N. Tandon4, David James Dyck5, Arend Bonen6, and Lawrence L. Spriet7

1 Human Health and Nutritional Sciences, University of Guelph, Guelph, Canada
2 Human Health and Nutritional Sciences, Univeristy of Guelph, Guelph, Canada
3 Department of Medicine, McMaster University Medical Center, Hamilton, Canada
4 Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories, Rockville, Maryland, United States
5 Human Health & Nutritional Sciences, University of Guelph, Guelph, Canada
6 Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Canada
7 Department of Human Health and Nutritional Science, University of Guelph, Guelph,, Canada

* To whom correspondence should be addressed. E-mail: ghollowa{at}uoguelph.ca.

A reduction in fatty acid oxidation has been associated with lipid accumulation and insulin resistance in the skeletal muscle of obese individuals. We examined whether this decrease in fatty acid oxidation was attributable to a reduction in muscle mitochondrial content and/or a dysfunction in fatty acid oxidation within mitochondria obtained from skeletal muscle of age-matched, lean (BMI = 23.3 ± 0.7 kg&#8729;m-2) and obese women (BMI = 37.6 ± 2.2 kg&#8729;m-2). The mitochondrial marker enzymes, citrate synthase (-34%), &#946;-hydroxyacyl-CoA dehydrogenase (-17%) and cytochrome c oxidase (-32%) were reduced (P<0.05) in obese participants, indicating mitochondrial content was diminished. Obesity did not alter the ability of isolated mitochondria to oxidize palmitate, however fatty acid oxidation was reduced at the whole muscle level by 28% (P<0.05) in the obese. Mitochondrial FAT/CD36 did not differ in lean and obese individuals, but mitochondrial FAT/CD36 was correlated with mitochondrial fatty acid oxidation (r=0.67, P<0.05). It is concluded that the reduction in fatty acid oxidation in obese individuals is attributable to a decrease in mitochondrial content, not to an intrinsic defect in the mitochondria obtained from skeletal muscle of obese individuals. In addition, it appears that mitochondrial FAT/CD36 may be involved in regulating fatty acid oxidation in human skeletal muscle.




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