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Effect of rosiglitazone treatment on circulating vascular and inflammatory markers in insulin-resistant subjects

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Fahim Abbasi

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Cynthia Lamendola

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Tracey McLaughlin

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Gerald M Reaven

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Philip S Tsao

Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305, US

Thiazolidinedione (TZD) compounds enhance insulin sensitivity and attenuate inflammation. The effect of the TZD compound, rosiglitazone (RSG) on both actions was evaluated in two groups of insulin-resistant subjects with minimal elevations of fasting plasma glucose (PG) concentration: group A (n=15, PG < 7.0 mmol/L) and group B (n=14, PG 7.0–8.3 mmol/L). Insulin action, quantified by the insulin suppression test, improved after three months of treatment in both groups, and concentrations of C-reactive protein, plasminogen activator inhibitor-1 and E-selectin all fell. Significant decreases in L-selectin and P-selectin were confined to group B, and concentrations of interleukin-6, intercellular adhesion molecule-1 and vascular cellular adhesion molecule-1 did not fall in either group.

Significant relationships were not discerned between enhanced insulin sensitivity and related variables and decreases in inflammatory/vascular markers, suggesting that RSG-induced changes in the latter variables in insulin-resistant individuals might be at least partly independent of the effects of the drug on insulin action.

Key Words: insulin resistance • inflammatory markers • thiazolidinedione compounds • insulin sensitivity • rosiglitazone

Diabetes and Vascular Disease Research, Vol. 2, No. 1, 37-41 (2005)
DOI: 10.3132/dvdr.2005.004


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