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Changes in Inflammation, Oxidative Stress, Mitochondrial DNA Content after Rosiglitazone in HIV Lipoatrophy | OMICS International | Abstract
ISSN 2155-6113

Journal of AIDS & Clinical Research
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Research Article

Changes in Inflammation, Oxidative Stress, Mitochondrial DNA Content after Rosiglitazone in HIV Lipoatrophy

Marisa Tungsiripat1, Dalia El-Bejjani1, Nesrine Rizk2, Bo Hu1, Allison C Ross2, Ulrich A Walker3,4, Dirk Lebrecht3, Ginger Milne5, Norma Storer2 and Grace A McComsey2*

1Cleveland Clinic, Cleveland, OH, USA

2Case Western Reserve University, Cleveland, OH, USA

3Albert-Ludwigs University, Freiburg, Germany

4Department of Rheumatology, Basel, Switzerland

5Vanderbilt University School of Medicine, Nashville, TN, USA

*Corresponding Author:
Grace A McComsey
Professor of Pediatrics and Medicine
Case School of Medicine Cleveland
OH 44106, USA
Tel: 2168443607
Fax: 2168448362
[email protected]

Received Date: August 30, 2012; Accepted Date: October 10, 2012; Published Date: October 15, 2012

Citation: Tungsiripat M, El-Bejjani D, Rizk N, Hu B, Ross AC, et al. (2012) Changes in Inflammation, Oxidative Stress, Mitochondrial DNA Content after Rosiglitazone in HIV Lipoatrophy. J AIDS Clinic Res 3:174. doi:10.4172/2155-6113.1000174

Copyright: © 2012 Tungsiripat M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Objective: We aim to evaluate the mechanisms of rosiglitazone-induced fat recovery in HIV+ patients with lipoatrophy on thymidine Nucleoside Reverse Transcriptase Inhibitors (NRTI) sparing regimens. Method: Measures of limb fat (DXA), oxidative stress (F2 isoprostanes) and inflammation [High-sensitivity C - reactive protein (hsCRP), soluble Tumor Necrosis Factor Receptors (sTNFR)-I, sTNFR-II, and interleukin (IL)-6] were performed. Gluteal fat mitochondrial DNA (mtDNA) and peroxisome proliferator-activated receptor (PPAR)-γ RNA [expressed as PPAR-γ/Glyceraldehyde 6-Phosphate Dehydrogenase (GAPDH) RNA ratio] were measured by quantitative PCR. Result: 71 patients on thymidine NRTI-sparing regimens were randomized to rosiglitazone vs. placebo for 48 weeks. Duration off thymidine NRTIs was similar between groups. From week 0-48, limb fat increased significantly (p=0.02) more in the rosiglitazone than in the placebo group. Within both groups, F2-isoprostanes, sTNFR-I and sTNFR-II increased significantly (p ≤ 0.003), hsCRP decreased significantly (≤ 0.02), and IL-6 did not change. No differences were seen between groups in any of the inflammation markers. Fat mtDNA (copies/ cell) increased nonsignificantly: +41(p=0.08) and +29(p=0.38) within rosiglitazone and placebo group; respectively. PPAR-γ/ GAPDH ratio did not change within or between groups. Conclusion: Limb fat improvements seen after rosiglitazone were not associated with changes in mtDNA, oxidative or inflammation markers, or PPAR-γ expression. F2 isoprostanes and some of the inflammation markers worsened over time in these subjects on stable ART, regardless of the rosiglitazone assignment. Thus, lipoatrophy can be in part overcome by a separate pathway independent of mitochondrial DNA depletion, such as PPAR-γ.


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