Regulation of skeletal muscle mitochondrial fatty acid metabolism in lean and obese individuals

摘要: A reduction in fatty acid (FA) oxidation has been associated with lipid accumulation and insulin resistance skeletal muscle of obese individuals. Numerous reports suggest that the FA may result from intrinsic mitochondrial defects, although little direct evidence offered to support this conclusion. This brief review summarizes recent work our laboratory reexamined whether decrease obesity was attributable a dysfunction within mitochondria or simply content. Whole-muscle content reduced obese, but there no ability isolated oxidize FA. The transport protein, translocase (FAT/CD36), did not differ between lean women correlated oxidation. It concluded is decreased defects oxidation, FAT/CD36 involved regulating human muscle. impaired biogenesis. However, protein contents various transcription factors, because peroxisome proliferater-activated receptor gamma coactivator 1alpha (PGC1alpha), PGC1beta, proliferator-activated alpha (PPARalpha), factor (TFAM) were obesity. In contrast, it appears altered regulation cofactors (PGC1alpha PGC1beta) their downstream factors (PPARalpha, PPARdelta/beta, TFAM), relations among these variables present individuals These findings imply would benefit interventions increase potential for oxidizing FAs.