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Relationship of Fat Distribution with Adipokines in Human Immunodeficiency Virus Infection

University of Colorado at Denver and Health Sciences Center (L.A.K.), Denver, Colorado 80217; University of California, San Francisco (P.B., M.G.S., C.G.), Veterans Affairs Medical Center (M.G.S., R.S., C.G.), San Francisco, California 94121; St. Luke’s-Roosevelt Hospital Center (D.P.K.), New York, New York 10025; Merck Research Laboratories (S.B.H.), Rahway, NJ 07065; and University of Alabama at Birmingham (C.E.L.), Birmingham, Alabama 35294

Address all correspondence and requests for reprints to: Carl Grunfeld, M.D., Ph.D., Office of the Principal Investigator, The FRAM Study, University of California, San Francisco, Veterans Affairs Medical Center, Metabolism Section 111F, 4150 Clement Street, San Francisco, California 94121. E-mail: carl.grunfeld{at}ucsf.edu.

Background and Methods: HIV-infected patients receiving antiretroviral therapy often develop changes in body fat distribution; the dominant change is reduction in sc adipose tissue (SAT). Because adipose tissue makes important hormones involved in whole-body energy metabolism, including leptin and adiponectin, we examined plasma concentrations and their relationship to regional adiposity measured by magnetic resonance imaging in 1143 HIV-infected persons (803 men and 340 women) and 286 controls (151 men and 135 women) in a cross-sectional analysis of the FRAM study.

Results: Total and regional adiposity correlated positively with leptin levels in HIV-infected subjects and controls (P < 0.0001). In controls, total and regional adiposity correlated negatively with adiponectin. In HIV-infected subjects, adiponectin was not significantly correlated with total adiposity, but the normal negative correlation with visceral adipose tissue and upper trunk SAT was maintained. However, leg SAT was positively associated with adiponectin in HIV-infected subjects. Within the lower decile of leg SAT for controls, HIV-infected subjects had paradoxically lower adiponectin concentrations compared with controls (men: HIV 4.1 µg/ml vs. control 7.5 µg/ml, P = 0.009; women: HIV 7.8 µg/ml vs. control 11.6 µg/ml, P = 0.037). Even after controlling for leg SAT, exposure to stavudine was associated with lower adiponectin, predominantly in those with lipoatrophy.

Conclusion: The normal relationships between adiponectin levels and total and leg adiposity are lost in HIV-infected subjects, possibly due to changes in adipocyte function associated with HIV lipodystrophy, whereas the inverse association of adiponectin and visceral adipose tissue is maintained. In contrast, the relationship between adiposity and leptin levels appears similar to controls and unaffected by HIV lipodystrophy.

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