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CLINICAL STUDY |
1 Department of Infectious Diseases, 2 Department of Internal Medicine and Endocrinology, 3 Clinical Research Unit and 4 Department of Clinical Biochemistry, Hvidovre University Hospital, Copenhagen, Denmark, 5 Copenhagen Muscle Research Centre/Department of Medical Physiology and 6 Department of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark and 7 Steno Diabetes Centre, Gentofte, University of Copenhagen, Copenhagen, Denmark
(Correspondence should be addressed to S B Haugaard, Clinical Research Unit 136, Hvidovre University Hospital, DK 2650 Hvidovre, Copenhagen, Denmark; Email: sbhau{at}dadlnet.dk)
Objectives: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and ß-cell function in lipodystrophic HIV-infected patients.
Methods: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naïve to antiretroviral therapy (NAÏVE) respectively). ß-cell function was evaluated by an intravenous glucose tolerance test.
Results: Compared with NONLIPO and NAÏVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; >34%, P < 0.001), hepatic insulin sensitivity (>40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAÏVE, indicating an impaired adaptation of ß-cell function to insulin resistance in LIPO.
Conclusion: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and ß-cell function.
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