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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Canada.
2 Presented at the symposium "The Emerging Interplay among Muscle Mitochondrial Function, Nutrition, and Disease" held at Experimental Biology 2008, San Diego, CA, 5 April 2008. 3 Supported by the Natural Sciences and Engineering Research Council of Canada (NSERCC; LLS and AB), the Canadian Institutes of Health Research (AB), and the Heart and Stroke Foundation of Canada (AB). AB holds a Canada Research Chair in Metabolism and Health. GPH was supported by an NSERCC graduate scholarship. 4 Reprints not available. Address correspondence to LL Spriet, Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada N1G 2W1. E-mail: lspriet{at}uoguelph.ca.
A reduction in fatty acid (FA) oxidation has been associated with lipid accumulation and insulin resistance in skeletal muscle of obese individuals. Numerous reports suggest that the reduction in FA oxidation may result from intrinsic mitochondrial defects, although little direct evidence has been offered to support this conclusion. This brief review summarizes recent work from our laboratory that reexamined whether this decrease in skeletal muscle FA oxidation with obesity was attributable to a dysfunction in FA oxidation within mitochondria or simply to a reduction in muscle mitochondrial content. Whole-muscle mitochondrial content and FA oxidation was reduced in the obese, but there was no decrease in the ability of isolated mitochondria to oxidize FA. The mitochondrial content of the transport protein, FA translocase (FAT/CD36), did not differ between lean and obese women but was correlated with mitochondrial FA oxidation. It was concluded that the reduced FA oxidation in obesity is attributable to decreased muscle mitochondrial content and not intrinsic defects in mitochondrial FA oxidation, and that mitochondrial FAT/CD36 is involved in regulating FA oxidation in human skeletal muscle. The reduced skeletal muscle mitochondrial content with obesity may result from impaired mitochondrial biogenesis. However, this did not result from decreased protein contents of various transcription factors, because peroxisome proliferater-activated receptor 
coactivator 1
(PGC1), PGC1β, peroxisome proliferator-activated receptor (PPAR), and mitochondrial transcription factor A (TFAM) were not reduced with obesity. In contrast, it appears that obesity is associated with altered regulation of cofactors (PGC1 and PGC1β) and their downstream transcription factors (PPAR, PPAR
/β, and TFAM), because relations among these variables were present in muscle from lean individuals but not from obese individuals. These findings imply that obese individuals would benefit from interventions that increase the skeletal muscle mitochondrial content and the potential for oxidizing FAs.
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