EFFECT OF ATANZANAVIR IN HIV PATIENTS WITH DYSLIPIDEMIA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Atazanavir, a recently approved protease inhibitor, has been associated with dyslipidemia. The mechanisms by which this protease inhibitor (PI) may result in improved lipid profiles is unknown. It is known that many HIV patients on PI-containing highly active antiretroviral therapy (HAART) can develop diabetes and/or dyslipidemia. there are several factors that can influence the development of these comorbidities, such as hepatic insulin resistance, high hepatic glucose output, and more recently, adipocytokines. Therefore, we want to determine the influence of atazanavir on these metabolic markers. The primary study objective is to quantify the portion of hepatic glucose production (HGP) derived from gluconeogenesis and glycogenolysis in the post-absorptive state and to determine insulin effects on gluconeogenesis using a three step hyperinsulinemic euglycemic clamp. Our secondary objectives are to 1) confirm the effect on the lipid profile when switching controlled HIV patient withs dyslipidemia on PI-containing HAART containing regimens to atazanavir containing HAART regimens; 2) determine changes in lipoprotein profile and effect on atherogenic dyslipidemia when switching therapy; 3) to quantify de novo lipogenesis in relationship to resting energy expenditure; 4) determine the effect of atazanavir on changes in adipocytokines as an indicator of fat metabolism regulation; 5) determine any changes in percent of body fat, lean body mass, and bone density on whole body DEXA scans; 6) determine any changes in whole body protein turnover.