In:
American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 297, No. 5 ( 2009-11), p. E1097-E1104
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0193-1849
,
1522-1555
DOI:
10.1152/ajpendo.90988.2008
Language:
English
Publisher:
American Physiological Society
Publication Date:
2009
detail.hit.zdb_id:
1477331-4
SSG:
12
