Abstract

Over one third of adults in the United States are obese. Skeletal muscle is a major site of metabolic activity and the most abundant tissue in the human body. For skeletal muscle to function at optimal levels, the efficient activation of processes that regulate muscle development, growth, regeneration and metabolism is required. Mitochondria play a key role in ensuring adequate levels of ATP needed for skeletal muscle contraction. In addition, the capacity of skeletal muscle to contribute to whole‐body energy expenditure is related to the fact that muscle makes up ~40% of total body mass and accounts for 20–30% of total resting oxygen uptake. This indicates that mitochondrial functional capacity is likely to directly affect muscle metabolic function and have a significant impact on whole‐body metabolism. Mitochondria are also important for ensuring muscle is able to modulate substrate oxidation (e.g. lipid and carbohydrate oxidation) following a meal. The objective of this study was to determine if there was an effect of body weight on genes related to mitochondrial function in skeletal muscle from normal weight (NW) and obese/overweight (OW) participants. Muscle biopsies were taken from OW (n=31, ages 48±19) and NW (n=12, ages 43±18) adults. Gene expression was measured using real‐time PCR. There was an increase (p<0.05) in the expression of both PGC1α and PPARγ, which are regulators of mitochondrial biogenesis, in OW vs NW participants. Expression of UCP2, a key regulator involved in ATP synthesis, was higher (p<0.05) in OW participants. In addition, genes related to mitochondrial respiration, mitochondrial DNA replication and transcription, NRF1 and Tfam, had higher (p<0.05) expression in OW. Cpt1a, a gene encoding carnitine palmitoyltransferase 1A, which is necessary for fatty acid oxidation, had lower (p<0.05) expression in OW compared with NW. Conclusively, these data provide a preliminary view of differences in energy metabolism gene expression in obese/overweight versus normal weight individuals.Support or Funding InformationArkansas Biosciences InstituteThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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