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Diabetes 51:797-802, 2002
© 2002 by the American Diabetes Association, Inc.

The Effects of Rosiglitazone on Insulin Sensitivity, Lipolysis, and Hepatic and Skeletal Muscle Triglyceride Content in Patients With Type 2 Diabetes

Adam B. Mayerson1, Ripudaman S. Hundal1, Sylvie Dufour1,3, Vincent Lebon1,3, Douglas Befroy1,3, Gary W. Cline1, Staffan Enocksson1, Silvio E. Inzucchi1, Gerald I. Shulman1,2,3, and Kitt F. Petersen1

1 Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut
2 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut
3 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut

We examined the effect of three months of rosiglitazone treatment (4 mg b.i.d.) on whole-body insulin sensitivity and in vivo peripheral adipocyte insulin sensitivity as assessed by glycerol release in microdialysis from subcutaneous fat during a two-step (20 and 120 mU · m-2 · min-1) hyperinsulinemic-euglycemic clamp in nine type 2 diabetic subjects. In addition, the effects of rosiglitazone on liver and muscle triglyceride content were assessed by 1H-nuclear magnetic resonance spectroscopy. Rosiglitazone treatment resulted in a 68% (P < 0.002) and a 20% (P < 0.016) improvement in insulin-stimulated glucose metabolism during the low- and high- dosage-insulin clamps, respectively, which was associated with ~40% reductions in plasma fatty acid concentration (P < 0.05) and hepatic triglyceride content (P < 0.05). These changes were associated with a 39% increase in extramyocellular lipid content (P < 0.05) and a 52% increase in the sensitivity of peripheral adipocytes to the inhibitory effects of insulin on lipolysis (P = 0.04). In conclusion, these results support the hypothesis that thiazolidinediones enhance insulin sensitivity in patients with type 2 diabetes by promoting increased insulin sensitivity in peripheral adipocytes, which results in lower plasma fatty acid concentrations and a redistribution of intracellular lipid from insulin responsive organs into peripheral adipocytes.


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