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Research Article| Volume 47, ISSUE 1, P52-58, July 2003

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Insulin resistance in HIV-infected patients: relationship with pro-inflammatory cytokines released by peripheral leukocytes

      Abstract

      Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-α and IL-1β) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients.
      Methods. Fourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured.
      Results. Plasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4±4.3 vs. 7.86±1.1 mIU, P=0.005; 2.27±0.91 vs. 1.6±0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-α concentrations in the supernatants of unstimulated PBMC cultures in HIV patients (Math Eq), but not in controls.
      Conclusions. Our results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-α, or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.

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