Energy Metabolism in Uncoupling Protein 3 Gene Knockout Mice *

  • Vidal-puig A
  • Grujic D
  • Zhang C
 et al. 
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Abstract

Uncoupling protein 3 (UCP3) is a member of the mito-chondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue dis-tribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and ther-moregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of re-active oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, produc-tion of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling ac-tivity and that its absence may lead to increased produc-tion of ROS. Despite these effects on mitochondrial func-tion, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phe-notypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alterna-tive compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined. Uncoupling protein 3 (UCP3) 1 (1–3) is a member of the

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Authors

  • Antonio J Vidal-puig

  • Danica Grujic

  • Chen-yu Zhang

  • Thilo Hagen

  • Olivier Boss

  • Yasuo Ido

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