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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/E1097    most recent 90988.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Blümer, R. M. E. Articles by Sauerwein, H. P. PubMed PubMed Citation Articles by Blümer, R. M. E. Articles by Sauerwein, H. P.

A rosiglitazone-induced increase in adiponectin does not improve glucose metabolism in HIV-infected patients with overt lipoatrophy

Departments of ¹Endocrinology and Metabolism and ²Infectious Diseases, Tropical Medicine and AIDS (Center for Infection and Immunity Amsterdam), ³International Antiviral Therapy Evaluation Center³ and the ⁴Department of Clinical Chemistry Laboratory of Endocrinology and Radiochemistry, Academic Medical Center, Amsterdam, The Netherlands

Submitted 10 December 2008 ; accepted in final form 28 July 2009

HIV-infected patients on antiretroviral therapy frequently develop changes in body fat distribution and disturbances in glucose metabolism, associated with reduced adiponectin levels. Because adiponectin, principally the high-molecular-weight (HMW) form, has insulin-sensitizing properties, we investigated the effects of an increase in adiponectin on glucose metabolism in HIV-lipodystrophy. In this randomized, double-blind, placebo-controlled trial, we included HIV-1-infected patients with severe lipoatrophy, with an undetectable viral load and who had received neither protease inhibitors nor stavudine for 6 mo. Patients were randomized to rosiglitazone [8 mg daily (n = 8)] to increase adiponectin levels or placebo (n = 5) for 16 wk. Peripheral glucose disposal, glucose production, and lipolysis were measured after an overnight fast and during a hyperinsulinemic-euglycemic clamp using stable isotopes. Body composition was assessed by computed tomography and dual-energy X-ray absorptiometry. Although body fat distribution was unaffected, rosiglitazone increased total plasma adiponectin levels by 107% (P < 0.02) and the ratio of HMW to total adiponectin by 73% (P < 0.001). In the placebo group, neither total adiponectin levels (P = 0.62) nor the ratio of HMW to total adiponectin changed (P = 0.94). The marked increase in adiponectin induced by rosiglitazone was not associated with significant changes in basal endogenous glucose production (P = 0.90), basal lipolysis (P = 0.90), insulin-mediated suppression of glucose production (P = 0.17) and lipolysis (P = 0.54) nor with changes in peripheral glucose disposal (P = 0.13). Acknowledging the limited statistical power of our small study, these findings, if confirmed by larger studies, could question the importance of adiponectin in regulating glucose metabolism in HIV-lipodystrophy.

insulin resistance; human immunodeficiency virus-associated lipodystrophy; adipocytokines