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Effect of Rosiglitazone on Peroxisome Proliferator‐Activated Receptor γ Gene Expression in Human Adipose Tissue Is Limited by Antiretroviral Drug–Induced Mitochondrial Dysfunction
Author(s) -
Patrick Mallon,
Rebecca Sedwell,
Gary David Rogers,
David Nolan,
Patrick Unemori,
Jennifer Hoy,
Katherine Samaras,
Anthony D. Kelleher,
Sean Emery,
David A. Cooper,
Andrew Carr
Publication year - 2008
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/593179
Subject(s) - lipoatrophy , rosiglitazone , adipose tissue , peroxisome proliferator activated receptor gamma , peroxisome proliferator activated receptor , endocrinology , medicine , mitochondrial toxicity , agonist , peroxisome , biology , receptor , toxicity , diabetes mellitus , virus , virology , viral load , antiretroviral therapy
Treatment of human immunodeficiency virus (HIV)-1 with thymidine-analogue nucleoside reverse-transcriptase inhibitors (tNRTIs) causes lipoatrophy, mitochondrial toxicity, and lower adipose tissue expression of peroxisome proliferator-activated receptor gamma (PPARgamma [PPARG gene]). Rosiglitazone (RSG), a PPARgamma agonist, improves congenital lipoatrophy but not HIV lipoatrophy.

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