Abstract | OBJECTIVE: Human immunodeficiency virus (HIV) patients on antiretroviral regimens frequently develop a syndrome of abnormal fat distribution, insulin resistance, and dyslipidemia. This lipodystrophic syndrome has been most closely linked to the use of HIV protease inhibitors (PIs). Several mechanisms have been postulated to explain these adverse effects of PIs, based largely on studies of rodent adipocytes. Intriguingly, atazanavir, a newer PI equally effective against HIV, is associated with fewer signs of lipodystrophy. We hypothesized that the less deleterious clinical effects of atazanavir would be reflected in physiological differences observed in PI-treated adipocytes. RESEARCH METHODS AND PROCEDURES: RESULTS: DISCUSSION: These data suggest that the distinct metabolic side effect profiles of these PIs could be a consequence of their differential effects on adipocyte physiology.
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Authors | Roy J Kim, Camella G Wilson, Martin Wabitsch, Mitchell A Lazar, Claire M Steppan |
Journal | Obesity (Silver Spring, Md.)
(Obesity (Silver Spring))
Vol. 14
Issue 6
Pg. 994-1002
(Jun 2006)
ISSN: 1930-7381 [Print] United States |
PMID | 16861604
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Adiponectin
- HIV Protease Inhibitors
- IL6 protein, human
- Insulin
- Interleukin-6
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Topics |
- Adipocytes
(drug effects)
- Adipogenesis
(drug effects, physiology)
- Adiponectin
(metabolism)
- Apoptosis
(drug effects)
- Cell Differentiation
(drug effects)
- Cells, Cultured
- HIV Protease Inhibitors
(adverse effects)
- Humans
- Insulin
(metabolism)
- Interleukin-6
(metabolism)
- Lipid Metabolism
(drug effects)
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