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PPAR Research
Volume 2009 (2009), Article ID 607902, 8 pages
Review Article

HIV-1 Infection and the PPAR -Dependent Control of Adipose Tissue Physiology

1Department of Biochemistry and Molecular Biology and Institute of Biomedicine, University of Barcelona, 08028 Barcelona, Spain
2CIBER Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, 08028 Barcelona, Spain
3Department of Internal Medicine, Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain

Received 5 May 2008; Accepted 23 July 2008

Academic Editor: Jacqueline Capeau

Copyright © 2009 Marta Giralt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


PPAR is a ligand-dependent master transcription factor controlling adipocyte differentiation as well as multiple biological processes taking place in other cells present in adipose tissue depots such as macrophages. Recent research indicates that HIV-1 infection-related events may alter adipose tissue biology through several mechanisms involving PPAR , ranging from direct effects of HIV-1-encoded proteins on adipocytes to the promotion of a proinflammatory environment that interferes with PPAR actions. This effect of HIV-1 on adipose tissue cells can occur even in the absence of direct infection of adipocytes, as soluble HIV-1-encoded proteins such as Vpr may enter cells and inhibit PPAR action. Moreover, repression of PPAR actions may relieve inhibitory pathways of HIV-1 gene transcription, thus enhancing HIV-1 effects in infected cells. HIV-1 infection-mediated interference of PPAR -dependent pathways in adipocytes and other cells inside adipose depots such as macrophages is likely to create an altered local environment that, after antiretroviral treatment, leads to lipodystrophy in HIV-1-infected and HAART-treated patients.