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HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms

Human immunodeficiency virus (HIV)-associated adipose redistribution syndrome (HARS) is a fat accumulation disorder characterized by increases in visceral adipose tissue. Patients with HARS may also present with excess truncal fat and accumulation of dorsocervical fat ("buffalo hump"). The...

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Detalles Bibliográficos
Autores principales: Lichtenstein, Kenneth, Balasubramanyam, Ashok, Sekhar, Rajagopal, Freedland, Eric
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934375/
https://www.ncbi.nlm.nih.gov/pubmed/17597538
http://dx.doi.org/10.1186/1742-6405-4-14
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author Lichtenstein, Kenneth
Balasubramanyam, Ashok
Sekhar, Rajagopal
Freedland, Eric
author_facet Lichtenstein, Kenneth
Balasubramanyam, Ashok
Sekhar, Rajagopal
Freedland, Eric
author_sort Lichtenstein, Kenneth
collection PubMed
description Human immunodeficiency virus (HIV)-associated adipose redistribution syndrome (HARS) is a fat accumulation disorder characterized by increases in visceral adipose tissue. Patients with HARS may also present with excess truncal fat and accumulation of dorsocervical fat ("buffalo hump"). The pathophysiology of HARS appears multifactorial and is not fully understood at present. Key pathophysiological influences include adipocyte dysfunction and an excessive free fatty acid release by adipocyte lipolysis. The contributory roles of free fatty acids, cytokines, hormones including cortisol, insulin and the growth hormone-adipocyte axis are significant. Other potential humoral, paracrine, endocrine, and neural influences are also discussed.
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spelling pubmed-19343752007-07-28 HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms Lichtenstein, Kenneth Balasubramanyam, Ashok Sekhar, Rajagopal Freedland, Eric AIDS Res Ther Review Human immunodeficiency virus (HIV)-associated adipose redistribution syndrome (HARS) is a fat accumulation disorder characterized by increases in visceral adipose tissue. Patients with HARS may also present with excess truncal fat and accumulation of dorsocervical fat ("buffalo hump"). The pathophysiology of HARS appears multifactorial and is not fully understood at present. Key pathophysiological influences include adipocyte dysfunction and an excessive free fatty acid release by adipocyte lipolysis. The contributory roles of free fatty acids, cytokines, hormones including cortisol, insulin and the growth hormone-adipocyte axis are significant. Other potential humoral, paracrine, endocrine, and neural influences are also discussed. BioMed Central 2007-06-27 /pmc/articles/PMC1934375/ /pubmed/17597538 http://dx.doi.org/10.1186/1742-6405-4-14 Text en Copyright © 2007 Lichtenstein et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Lichtenstein, Kenneth
Balasubramanyam, Ashok
Sekhar, Rajagopal
Freedland, Eric
HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title_full HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title_fullStr HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title_full_unstemmed HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title_short HIV-associated adipose redistribution syndrome (HARS): etiology and pathophysiological mechanisms
title_sort hiv-associated adipose redistribution syndrome (hars): etiology and pathophysiological mechanisms
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934375/
https://www.ncbi.nlm.nih.gov/pubmed/17597538
http://dx.doi.org/10.1186/1742-6405-4-14
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