HIV-1 can induce disturbances in adipose tissue in infected subjects through the effects of some of its proteins or inflammation. It is not known whether this also takes place in HIV-1–infected long-term nonprogressors (LTNPs). Our objectives were to determine whether adipocyte differentiation/lipid, inflammatory, and mitochondrial parameters are perturbed in abdominal wall subcutaneous adipose tissue of untreated HIV-1–infected patients LTNPs.
Cross-sectional study involving 10 LTNPs, 10 typical progressors (TPs), and 10 uninfected controls (UCs). The parameters assessed were peroxisome proliferator–activated receptor-gamma (PPARγ), lipoprotein lipase, and fatty acid–binding protein 4 mRNA (adipogenic/lipid); tumor necrosis factor-alpha, interleukin 18 (IL-18), β2-MCG, monocyte chemoattractant protein 1, CD1A, and C3 mRNA (inflammation); and cytochrome c oxidase subunit II (COII), COIV, CYCA, nuclear respiratory factor 1, PPARγ coactivator 1α mRNA, and mtDNA content (mitochondrial).
Regarding adipogenic/lipid parameters, LTNPs had PPARγ, lipoprotein lipase, and fatty acid–binding protein 4 mRNA significantly decreased compared with UCs (P ≤ 0.001 for all comparisons). PPARγ mRNA was significantly greater in LTNP than in TP (P = 0.006). With respect to inflammatory parameters, tumor necrosis factor-alpha, IL-18, and β2-MCG mRNA were significantly higher in LTNPs compared with UCs (P < 0.005 for all comparisons), whereas IL-18 mRNA was greater in TPs compared with LTNPs (P = 0.01). As mitochondrial parameters are concerned, mtDNA was significantly reduced in LTNPs compared with TPs (P = 0.04) and UCs (P = 0.03). COII and COIV were also significantly reduced in LTNPs compared with UCs and TPs.
Adipose tissue from untreated LTNPs may have limited but significant derangements in some adipogenic/lipid and may have inflammatory processes at a lower degree than that observed in untreated TPs. LTNPs may have mitochondrial-related alterations in adipose tissue which are greater than that observed in TPs.
*Department of Internal Medicine, Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, Tarragona, Spain
†Department of Internal Medicine, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain
‡Departament de Bioquímica i Biologia Molecular, Institut de Biomedicina, Universitat de Barcelona and CIBER Fisiopatología de la Obesidad y Nutrición, Barcelona, Spain.
Correspondence to: Francesc Vidal, MD, PhD, Infectious diseases and HIV/AIDS Unit, Department of Internal Medicine, Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, Mallafré Guasch, 4, 43007 Tarragona, Spain (e-mail: email@example.com).
Supported by Instituto de salud Carlos III grants PI07/0976, PI08/1715, and PI10/2635, PI11/0376 and INT11/240. Fondos para el Desarrollo Europeo Regional; Programa de suport als grups de recerca AGAUR (2009) grants SGR 284, 959, and 1061; Ministerio de Ciencia e Innovación grant SAF2008-02278, SAF2012-35198; Ministerio de Sanidad, Política Social e Igualdad grant EC11-293; Red de Investigación en Sida grants RIS, RD06/006/0022 and RD06/0006/1004, ISCIII, Spain.
The authors have no conflicts of interest to disclose.
Received January 26, 2012
Accepted April 13, 2012