Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats

V. Saengsirisuwan, T. R. Kinnick, M. B. Schmit, E. J. Henriksen

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

Exercise training (ET) or the antioxidant R(+)-α-lipoic acid (R-ALA) individually increases insulin action in the insulin-resistant obese Zucker rat. The purpose of the present study was to determine the interactions of ET and R-ALA on insulin action and oxidative stress in skeletal muscle of the obese Zucker rat. Animals either remained sedentary, received R-ALA (30 mg·kg body wt-1·day-1), performed ET (treadmill running), or underwent both R-ALA treatment and ET for 6 wk. During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose (26-32%) and insulin (29-30%) responses compared with sedentary controls. R-ALA alone decreased (19%) the glucose-insulin index (indicative of increased insulin sensitivity), and this parameter was reduced (48-52%) to the greatest extent in the ET and combined treatment groups. ET or R-ALA individually increased insulin-mediated glucose transport activity in isolated epitrochlearis (44-48%) and soleus (37-57%) muscles. The greatest increases in insulin action in these muscles (80 and 99%, respectively) were observed in the combined treatment group. Whereas the improvement in insulin-mediated glucose transport in soleus due to R-ALA was associated with decreased protein carbonyl levels (an index of oxidative stress), improvement because of ET was associated with decreased protein carbonyls as well as enhanced GLUT-4 protein. However, there was no interactive effect of ET and R-ALA on GLUT-4 protein or protein carbonyl levels. These results indicate that ET and R-ALA interact in an additive fashion to improve insulin action in insulin-resistant skeletal muscle. Because the further improvement in muscle glucose transport in the combined group was not associated with additional upregulation of GLUT-4 protein or a further reduction in oxidative stress, the mechanism for this interaction must be due to additional, as yet unidentified, factors.

Original languageEnglish (US)
Pages (from-to)145-153
Number of pages9
JournalJournal of Applied Physiology
Volume91
Issue number1
DOIs
StatePublished - 2001

Keywords

  • GLUT-4 protein
  • Glucose tolerance
  • Insulin resistance
  • Oxidative stress
  • Protein carbonyls

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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