Getting to the HAART of insulin resistance
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There is now abundant evidence that HIV protease inhibitors (PI) as a class make a powerful independent contribution to the 'metabolic syndrome' that accompanies the long-term use of highly active antiretroviral therapy (HAART) regimens. Clinical studies have demonstrated that PI therapy is strongly associated with the development of dyslipidemia and insulin resistance [1-6], and that short-term use of PI is sufficient to cause these abnormalities even in the absence of body composition changes associated with the 'lipodystrophy syndrome'. Two published studies involving HIV-seronegative individuals have also shown that HIV infection is not a prerequisite condition for the effects of PI on lipid and glucose metabolism [8,9]. However, there are a number of critical questions that remain unresolved at this time. Firstly, what is the relationship between PI therapy and the three components of the 'metabolic syndrome' - dyslipidemia, insulin resistance, and visceral adiposity - and which of these interrelated outcomes is the primary pathogenic event? Secondly, how do PI, or the metabolic syndrome they cause, interact with nucleoside analogue reverse transcriptase inhibitors (NRTI) in the pathogenesis of subcutaneous fat wasting in individuals with lipodystrophy? The answers to these questions are fundamental to an understanding of the pathogenesis of the HIV lipodystrophy syndrome. In this setting, the study presented by Kosmiski et al. in this issue of AIDS provides some welcome insights.
|Publication Type:||Journal Article|
|Murdoch Affiliation:||Centre for Clinical Immunology and Biomedical Statistics|
|Publisher:||Lippincott Williams & Wilkins Ltd.|
|Copyright:||© 2001 Lippincott Williams & Wilkins, Inc.|
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