4.3 Article

Lipodystrophy and Insulin Resistance in Combination Antiretroviral Treated HIV-1-Infected Patients: Implication of Resistin

Journal

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAI.0b013e318213312c

Keywords

HIV; combination antiretroviral therapy; lipodystrophy; resistin; insulin resistance

Funding

  1. Fondo de Investigacion Sanitaria [07/0976, 08/1032, 08/1195, 10/2635]
  2. Fondos para el Desarrollo Europeo Regional (FEDER)
  3. Fundacion para la Investigacion y Prevencion del Sida en Espana [FIPSE 06/36572, 06/30610, 36-0998-10]
  4. Ministerio de Ciencia e Innovacion
  5. Programa de Suport als Grups de Recerca AGAU [2009 SGR 959, 1061, 1257]
  6. Red de Investigacion en Sida (RIS) [RD06/006/0022, RD06/0006/1004]
  7. ISCIII
  8. Ministerio de Sanidad y Consumo, Spain
  9. Juan de la Cierva (JDC) [JDCI20071020]
  10. [SAF2008-02278]

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Background: 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. Methods: 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 -420>C. G was assessed using restriction fragment length polymorphism. Student t test, 1-way and 2-way analysis of variance, chi(2) test, and Pearson and Spearman correlations were performed for statistical analysis. Results: 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. Conclusions: In our cohort of white Spaniards, the rest -420>C. G single-nucleotide polymorphism may be associated with cART-related lipodystrophy. Plasma resistin correlates with insulin resistance in infected patients with and without lipodystrophy.

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