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Circulating Resistin Levels Are Not Associated with Fat Redistribution, Insulin Resistance, or Metabolic Profile in Patients with the Highly Active Antiretroviral Therapy-Induced Metabolic Syndrome

Divisions of Endocrinology, Diabetes, and Metabolism (D.B., A.G., J.L.C., C.J.W., C.S.M.) and Infectious Disease (S.G.W., A.W.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215; and Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig (J.K.), 04109 Leipzig, Germany

Address all correspondence and requests for reprints to: Dr. Christos S. Mantzoros, Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Stoneman 816, Boston, Massachusetts 02215. E-mail: cmantzor{at}bidmc.harvard.edu.

Context: The mechanisms underlying the development of the highly active antiretroviral therapy (HAART)-induced metabolic syndrome remain to be fully elucidated.

Objective: The objective of this study was to investigate whether the adipocyte-secreted hormone, resistin, is associated with anthropometric and metabolic abnormalities of the HAART-induced metabolic syndrome.

Design, Setting, and Patients: We conducted a cross-sectional study of 227 HIV-positive patients (37 women and 190 men) recruited from the infectious diseases clinics. On the basis of history, physical examination, dual-energy x-ray absorptiometry, and single-slice computed tomography, patients were classified into four groups: non-fat redistribution (n = 85), fat accumulation (n = 42), fat wasting (n = 35), and mixed fat redistribution (n = 56).

Main Outcome Measures: The main outcome measures were serum resistin levels and anthropometric and metabolic variables.

Results: Mean serum resistin levels were not significantly different among subjects with fat accumulation, fat wasting, or mixed fat redistribution or between these groups and the non-fat redistribution group. We found a weak, but significant, positive correlation between resistin and percent total body fat (r = 0.20; P < 0.01), total extremity fat (r = 0.18; P < 0.01), and abdominal sc fat (r = 0.19; P < 0.01), but not abdominal visceral fat (r = –0.10; P = 0.16) or waist to hip ratio (r = –0.05; P = 0.43). When adjustments were made for gender (women, 3.92 ± 2.71 ng/ml; men, 2.96 ± 2.61 ng/ml; P = 0.05), correlations between resistin and the above parameters were no longer significant. Importantly, resistin levels were not correlated with fasting glucose, insulin, homeostasis model assessment of insulin resistance index, triglycerides, or cholesterol levels in the whole group.

Conclusions: Resistin is related to gender, but is unlikely to play a major role in the insulin resistance and metabolic abnormalities of the HAART-induced metabolic syndrome.