Abstract
PPARγ 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 PPARγ, ranging from direct effects of HIV-1-encoded proteins on adipocytes to the promotion of a proinflammatory environment that interferes with PPARγ 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 PPARγ action. Moreover, repression of PPARγ actions may relieve inhibitory pathways of HIV-1 gene transcription, thus enhancing HIV-1 effects in infected cells. HIV-1 infection-mediated interference of PPARγ-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.
Highlights
A complex set of metabolic alterations, preferentially involving adipose tissue, has emerged in recent years in a substantial number of HIV-1-infected patients under highly-active antiretroviral treatment (HAART)
The precise mechanisms of action of peroxisome proliferator-activated receptor γ (PPARγ) on HIV-1 are not fully known and, in addition to the potential direct interaction with specific regions of the long-terminal repeat mentioned above, indirect effects via nuclear factor κB have been proposed on the basis of the effects of PPARγ and its ligand rosiglitazone impairing nuclear factor κB-mediated enhancement of HIV1 replication in macrophages [84]. All these findings indicate the occurrence of a potential cross-talk between PPARγ and HIV-1 that could reinforce the activity of HIV-1 proteins in cells harboring PPARγ
Research to date indicates that HIV-1 infectionrelated events may alter adipose tissue and contribute to development of the full-blown lipodystrophy syndrome after antiretroviral treatment
Summary
A complex set of metabolic alterations, preferentially involving adipose tissue, has emerged in recent years in a substantial number of HIV-1-infected patients under highly-active antiretroviral treatment (HAART). This is the so-called HIV1/HAART-associated lipodystrophy syndrome. Regardless of the potential effects of antiretroviral drugs on PPARγ, several recent findings suggest that HIV-1 infection-related events may cause disturbances in the PPARγ-dependent pathways of control of adipose tissue physiopathology, and they are summarized in the present review. Disturbances of PPARγ, as a master regulator of adipose tissue differentiation and function, may play a major role in the alterations of adipose mass and lipid metabolism elicited by HIV-1 infection, and this issue is summarized in the present review
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