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Wiley InterScience | |||||||||
![]() Clinical & Experimental ImmunologyVolume 135 Issue 2, Pages 273 - 279 Published Online: 22 Jan 2004 Journal Compilation © 2010 British Society for Immunology An Official Journal of the British Society for Immunology
Abstract | References | Full Text: HTML, PDF (Size: 96K) | Related Articles | Citation Tracking Low plasma level of adiponectin is associated with stavudine treatment and lipodystrophy in HIV-infected patients Copyright 2004 Blackwell Publishing Ltd KEYWORDS HIV • lipodystrophy • insulin resistance • adiponectin • cytokines SUMMARY
This study tested the hypothesis that in patients with HIV-associated lipodystrophy, adiponectin levels were related to insulin resistance, TNF-α and IL-6 and treatment with nucleoside analaogues. HIV seropositive men undergoing highly active antiretroviral treatment were enrolled into three predetermined clinical groups: lipodystrophy with central fat accumulation (n = 12); lipodystrophy without central fat accumulation (n = 15); no lipodystrophy (n = 15). HIV-negative healthy men served as controls (n = 12). Both lipodystrophic groups had a low percentage of limb fat compared to the two control groups. Patients with lipodystrophy with fat accumulation had increased truncal fat compared with controls. Levels of adiponectin did not correlate with either TNF-α or IL-6. Low levels of adiponectin were found in both lipodystrophic groups and were associated with current or previous treatment with stavudine. Furthermore, the adiponectin level correlated with the percentage of limb fat. Patients with lipodystrophy with fat accumulation were more insulin resistant, measured by HOMA-IR, compared with controls. However, HOMA-IR did no correlate to adiponectin or other cytokines. In conclusion, the finding of no difference between the two lipodystrophic groups with regard to adiponectin, indicates that low levels of adiponectin reflects fat atrophy, whereas the insulin resistance was best explained by increased truncal fat mass. (Accepted for publication 28 November 2003) |