Mitochondrial Respiratory Capacity and Content Are Normal in Young Insulin-Resistant Obese Humans

  1. P. Darrell Neufer1,2,3
  1. 1East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC
  2. 2Department of Physiology, East Carolina University, Greenville, NC
  3. 3Department of Kinesiology, East Carolina University, Greenville, NC
  4. 4Department of Health and Kinesiology, Purdue University, West Lafayette, IN
  1. Corresponding author: P. Darrell Neufer, neuferp{at}ecu.edu.
  1. K.H.F.-W. and T.M.W. contributed equally to this work.

Abstract

Considerable debate exists about whether alterations in mitochondrial respiratory capacity and/or content play a causal role in the development of insulin resistance during obesity. The current study was undertaken to determine whether such alterations are present during the initial stages of insulin resistance in humans. Young (∼23 years) insulin-sensitive lean and insulin-resistant obese men and women were studied. Insulin resistance was confirmed through an intravenous glucose tolerance test. Measures of mitochondrial respiratory capacity and content as well as H2O2 emitting potential and the cellular redox environment were performed in permeabilized myofibers and primary myotubes prepared from vastus lateralis muscle biopsy specimens. No differences in mitochondrial respiratory function or content were observed between lean and obese subjects, despite elevations in H2O2 emission rates and reductions in cellular glutathione. These findings were apparent in permeabilized myofibers as well as in primary myotubes. The results suggest that reductions in mitochondrial respiratory capacity and content are not required for the initial manifestation of peripheral insulin resistance.

  • Received June 15, 2013.
  • Accepted August 15, 2013.

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  1. Diabetes vol. 63 no. 1 132-141
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