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Division of Biological Sciences and Department of Nutrition (Q.T., G.T., G.S.H.), and Department of Immunology and Infectious Diseases (J.-L.S., P.J.K.), Harvard School of Public Health, Boston, Massachusetts 02115; and Combined Program in Pediatric Gastroenterology and Nutrition (C.M.H., S.K.G.), Program in Nutritional Metabolism (C.M.H., S.K.G.), and Division of Infectious Disease (E.S.R.), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
Address all correspondence and requests for reprints to: Dr. Gökhan S. Hotamisligil, Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115. E-mail: ghotamis{at}hsph.harvard.edu; or Dr. Steven K. Grinspoon, Director, Program in Nutritional Metabolism, Massachusetts General Hospital, Harvard Medical School, LON207, Fruit Street, Boston, Massachusetts 02114. E-mail: sgrinspoon{at}partners.org.
HIV-related lipodystrophy is characterized by adipose redistribution, dyslipidemia, and insulin resistance. Adiponectin is an adipose-derived peptide thought to act as a systemic regulator of glucose and lipid metabolism. We investigated adiponectin concentrations in 10 HIV-infected patients during acute HIV infection (viral load, 2.0 x 106 ± 1.0 x 106 copies/ml) and then 6–8 months later, as well as cross-sectionally in 41 HIV-infected patients (21 with evidence of fat redistribution and 20 without evidence of fat redistribution) in comparison with 20 age- and body mass index-matched healthy control subjects. Circulating adiponectin concentrations did not change with treatment of acute HIV infection (5.8 ± 0.4 vs. 5.9 ± 0.7 µg/ml, P = 0.96) but were reduced in patients with chronic HIV infection and fat redistribution (7.8 ± 0.9 µg/ml), compared with age- and body mass index-matched HIV-infected patients without fat redistribution (12.7 ± 1.7 µg/ml) and healthy control subjects (11.9 ± 1.7 µg/ml, P < 0.05 vs. HIV-infected patients without fat redistribution and vs. control subjects). Adiponectin concentrations correlated with body composition [correlation coefficient (r) = -0.47, P = 0.002 vs. trunk fat:total fat; r = 0.51, P < 0.001 vs. extremity fat:total fat], insulin response to glucose challenge (r = -0.36, P = 0.03), triglyceride (r = -0.39, P = 0.01), and high-density lipoprotein (r = 0.37, P = 0.02) among the HIV-infected patients. Adiponectin remained a significant correlate of insulin response to GTT, controlling for medication use and body composition changes in HIV-infected patients. These data suggest a strong relationship between adiponectin and body composition in HIV-infected patients. Changes in adiponectin may contribute to the metabolic dysregulation in this group of patients.
This work was supported by Grant R01-DK-59535 (to S.K.G.), NIH Grants AI-43879 and AI-467274 (to F.J.K.), and a research grant (to G.H.S.) from Bristol-Myers Squibb Co. Pharmaceutical Research Institute (Princeton, NJ).
Abbreviations: AUC, Area under the curve; BMI, body mass index; CT, computed tomography; DEXA, dual-energy x-ray absorptiometry; HAART, highly active antiretroviral therapy; HDL, high-density lipoprotein; LDL, low-density lipoprotein; NRTI, nonnucleoside reverse transcriptase inhibitor; PI, protease inhibitor; SAT, sc adipose tissue; TAT, total abdominal cross-sectional area; VAT, visceral adipose tissue.
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