Reduced skeletal muscle mitochondrial content and fatty acid oxidation are associated with obesity and insulin resistance. While the exact mechanisms remain elusive, this may result from impaired mitochondrial biogenesis, or reductions in the mitochondrial reticulum network. Therefore, the purpose of this study was to determine if the protein contents of various transcription factors, including PGC1 and PGC1, and proteins associated with mitochondrial fusion events, were reduced in skeletal muscle of nine obese (BMI=37.6±2.2 kg/m^-2) compared to nine, age-matched lean (BMI=23.3±0.7 kg/m^-2) women. The protein contents of PGC1, PGC1,PPAR and tFAM were not reduced with obesity. In contrast, PPAR was increased (+22%, P<0.05) with obesity, and there was a trend towards an increase (+31%, P=0.13) in PPAR/. In lean individuals, PGC1 protein correlated with citrate synthase (CS; r=0.67) and rates of palmitate oxidation (r=0.87), while PGC1 correlated with PPAR (r=0.90), PPAR/ (r=0.63), and cytochrome c oxidase IV (COXIV; r=0.63). In obese individuals the relationship between PGC1 and CS was maintained (r=0.65); however, the associations between PGC1 and palmitate oxidation (r=-0.38), and PGC1 with PPAR (r=0.14), PPAR/ (r=0.21) and COXIV (r=0.01) were lost. In addition, Mitofusin-1 (MFN-1), MFN-2, and dynamin-related protein 1 (DRP-1) total protein contents were not altered with obesity (P>0.05). These data suggest that altered regulation, and not reductions in the protein contents of transcription factors are associated with insulin resistance. Also, it does not appear that alterations in the proteins associated with mitochondrial network formation and degradation can account for the observed decrease in mitochondrial content.