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Diabetes 52:1311-1318, 2003
© 2003 by the American Diabetes Association, Inc.

Differential Effects of Rosiglitazone on Skeletal Muscle and Liver Insulin Resistance in A-ZIP/F-1 Fatless Mice

Jason K. Kim1, Jonathan J. Fillmore1, Oksana Gavrilova2, Lily Chao2, Takamasa Higashimori1, Hyejeong Choi1, Hyo-Jeong Kim1, Chunli Yu1, Yan Chen3, Xianqin Qu4, Martin Haluzik2, Marc L. Reitman2, and Gerald I. Shulman1,3,5

1 Department of Internal Medicine, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut
2 Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland
3 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut
4 Department of Health Sciences, University of Technology, Sydney, New South Wales, Australia
5 Department of Cellular and Molecular Physiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut

To determine the role of adipocytes and the tissue-specific nature in the insulin sensitizing action of rosiglitazone, we examined the effects of 3 weeks of rosiglitazone treatment on insulin signaling and action during hyperinsulinemic-euglycemic clamps in awake A-ZIP/F-1 (fatless), fat-transplanted fatless, and wild-type littermate mice. We found that 53 and 66% decreases in insulin-stimulated glucose uptake and insulin receptor substrate (IRS)-1–associated phosphatidylinositol (PI) 3-kinase activity in skeletal muscle of fatless mice were normalized after rosiglitazone treatment. These effects of rosiglitazone treatment were associated with 50% decreases in triglyceride and fatty acyl-CoA contents in the skeletal muscle of rosiglitazone-treated fatless mice. In contrast, rosiglitazone treatment exacerbated hepatic insulin resistance in the fatless mice and did not affect already reduced IRS-2–associated PI 3-kinase activity in liver. The worsening of insulin action in liver was associated with 30% increases in triglyceride and fatty acyl-CoA contents in the liver of rosiglitazone-treated fatless mice. In conclusion, these data support the hypothesis that rosiglitazone treatment enhanced insulin action in skeletal muscle mostly by its ability to repartition fat away from skeletal muscle.


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