Little information is available with respect to the involvement of resistin in lipodystrophy and metabolic disturbances in HIV-1-infected patients treated with combination antiretroviral therapy (cART). We determined whether the resistin (rest) −420C>G single-nucleotide polymorphism and plasma resistin are associated with the development of lipodystrophy and metabolic disturbances in HIV-1-infected patients treated with cART.
The study group comprised 299 HIV-1-infected patients treated with a stable cART for at least 1 year (143 with lipodystrophy and 156 without) and 175 uninfected controls. Anthropometric, clinical, and metabolic variables were determined. Homeostasis model assessment for insulin resistance was used to evaluate insulin resistance. Plasma resistin levels were determined by enzyme-linked immunosorbent assay. The rest −420C>G was assessed using restriction fragment length polymorphism. Student t test, 1-way and 2-way analysis of variance, χ2 test, and Pearson and Spearman correlations were performed for statistical analysis.
Genotypes containing the rest −420G variant allele were significantly more common in HIV-1-infected patients without lipodystrophy compared with those with lipodystrophy (P = 0.037). Infected patients had significantly greater plasma resistin levels than uninfected controls (P < 0.001). Among infected patients, plasma resistin levels were significantly lower in patients with lipodystrophy with respect to those without (P = 0.034). In infected patients, plasma resistin levels had a significant positive correlation with insulin and homeostasis model assessment for insulin resistance: P < 0.001 and P = 0.002 in the lipodystrophy subset and P = 0.002 and P = 0.03 in the nonlipodystrophy subset, respectively.
In our cohort of white Spaniards, the rest −420C>G single-nucleotide polymorphism may be associated with cART-related lipodystrophy. Plasma resistin correlates with insulin resistance in infected patients with and without lipodystrophy.
From the *Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, Tarragona, Spain; †CIBER Diabetes y Enfermedades Metabólicas Asociadas (CIBERdem), Instituto de Salud Carlos III, Barcelona, Spain; ‡Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain; and §Hospital Universitari de Sant Joan, Reus, IISPV, Universitat Rovira i Virgili, Reus, Spain.
Received for publication October 16, 2010; accepted January 28, 2011.
This work was partially financed by grants from the Fondo de Investigacion Sanitaria (07/0976, 08/1032, 08/1195, 10/2635); Fondos para el Desarrollo Europeo Regional (FEDER); Fundación para la Investigación y Prevención del Sida en España (FIPSE 06/36572, 06/30610 and 36-0998-10); SAF2008-02278, Ministerio de Ciencia e Innovación; Programa de Suport als Grups de Recerca AGAUR (2009 SGR 959, 1061 and 1257); and Red de Investigación en Sida (RIS, RD06/006/0022 and RD06/0006/1004), ISCIII, Ministerio de Sanidad y Consumo, Spain.
X. Escoté is supported by a fellowship from the Juan de la Cierva (JDC) program (JDCI20071020).
X. Escoté, M. Miranda, and S. Veloso have contributed equally to this work.
The authors have no funding or conflicts of interest to disclose.
Correspondence to: Francesc Vidal, MD, PhD, Infectious Diseases and HIV/AIDS Section, Department of Internal Medicine, Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, Mallafré Guasch, 4, 43007 Tarragona, Spain (e-mail: email@example.com).