4th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 22-25 September 2002, San Diego, CA, USA

DIRECT REGULATION OF ADIPONECTIN BY HIV AND ITS LINK TO LIPODYSTROPHY

Antiviral Therapy 2002; 7:L23 (abstract 32)

Q Tong¹, J-L Sankalé², CM Hadigan³, G Tan¹, ES Rosenberg⁴, PJ Kanki², SK Grinspoon³, GS Hotamisligil^1
1Division of Biological Sciences and Department of Nutrition; ²Department of Immunology & Infectious Diseases, Harvard School of Public Health; ³Program In Nutritional Metabolism; ⁴Division of Infectious Disease, Massachusetts General Hospital, Harvard Medical School, Boston, USA

HIV-related lipodystrophy is characterized by adipose redistribution, dyslipidaemia, and insulin resistance. The underlying molecular mechanisms remain largely unknown. In this study, we have demonstrated that adipocytes express HIV receptors. Although we found no evidence of HIV entry or amplification in human adipocytes or preadipocytes, our data demonstrate that exposure to HIV virus stimulates the secretion of adiponectin from human adipocytes. We also demonstrate that T lymphocytes produce adiponectin, but adiponectin production is suppressed upon T-cell activation. Finally, we demonstrate that adiponectin concentrations are significantly reduced in HIV patients with lipodystrophy compared to age and BMI-matched HIV patients without lipodystrophy and healthy controls. Reduced adiponectin concentrations are strongly correlated with adipose tissue redistribution, insulin resistance, and dyslipidaemia (increased triglyceride and decreased HDL) and are an independent predictor of hyperinsulinaemia in HIV-infected patients. These are the first data to suggest the potential molecular mechanisms by which adiponectin is regulated in HIV-infected patients. Reduced adiponectin levels may contribute to hyperinsulinaemia and insulin resistance in this population and present a novel therapeutic opportunity.

Presenting author: Q Tong

2002-09-22
32

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