Oxidative damage associated with obesity is prevented by overexpression of CuZn- or Mn-superoxide dismutase

Yuhong Liu, Wenbo Qi, Arlan Richardson, Holly Van Remmen, Yuji Ikeno, Adam B. Salmon

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

The development of insulin resistance is the primary step in the etiology of type 2 diabetes mellitus. There are several risk factors associated with insulin resistance, yet the basic biological mechanisms that promote its development are still unclear. There is growing literature that suggests mitochondrial dysfunction and/or oxidative stress play prominent roles in defects in glucose metabolism. Here, we tested whether increased expression of CuZn-superoxide dismutase (Sod1) or Mn-superoxide dismutase (Sod2) prevented obesity-induced changes in oxidative stress and metabolism. Both Sod1 and Sod2 overexpressing mice were protected from high fat diet-induced glucose intolerance. Lipid oxidation (F2-isoprostanes) was significantly increased in muscle and adipose with high fat feeding. Mice with increased expression of either Sod1 or Sod2 showed a significant reduction in this oxidative damage. Surprisingly, mitochondria from the muscle of high fat diet-fed mice showed no significant alteration in function. Together, our data suggest that targeting reduced oxidative damage in general may be a more applicable therapeutic target to prevent insulin resistance than is improving mitochondrial function.

Original languageEnglish (US)
Pages (from-to)78-83
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume438
Issue number1
DOIs
StatePublished - Aug 16 2013

    Fingerprint

Keywords

  • Diabetes
  • F-isoprostane
  • Mitochondria
  • Oxidative stress

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this