Adipose tissue biology and HIV-infection

被引:56
作者
Giralt, Marta [1 ,2 ,3 ]
Domingo, Pere [4 ,5 ]
Villarroya, Francesc [2 ,3 ]
机构
[1] Univ Barcelona, Fac Biol, Dept Biochem & Mol Biol, E-08028 Barcelona, Catalonia, Spain
[2] Univ Barcelona, Inst Biomed IBUB, E-08028 Barcelona, Catalonia, Spain
[3] Inst Salud Carlos III, CIBER Fisiopatol Obesidad & Nutr, Barcelona, Spain
[4] Hosp Santa Creu & Sant Pau, Infect Dis Unit, Barcelona, Catalonia, Spain
[5] Inst Salud Carlos III, Red Invest SIDA RIS, Barcelona, Spain
关键词
adipose; adipokine; adipocyte; HIV-1; lipodystrophy; antiretroviral; REVERSE-TRANSCRIPTASE INHIBITORS; NECROSIS-FACTOR-ALPHA; INSULIN-RESISTANCE; ANTIRETROVIRAL-THERAPY; GENE-EXPRESSION; ADIPOCYTE DIFFERENTIATION; PROTEASE INHIBITORS; IN-VITRO; HIV-1-INFECTED PATIENTS; FAT REDISTRIBUTION;
D O I
10.1016/j.beem.2010.12.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
HIV-1/highly active antiretroviral therapy-associated lipodystrophy syndrome (HALS) is an adipose tissue redistribution disorder characterized by subcutaneous adipose tissue lipoatrophy, sometimes including visceral adipose tissue hypertrophy and accumulation of dorsocervical fat ('buffalo hump'). The pathophysiology of HALS appears to be multifactorial and several key pathophysiological factors associated with HALS have been identified. These include mitochondrial dysfunction, adipocyte differentiation disturbances, high adipocyte lipolysis, and adipocyte apoptosis. These alterations in adipose tissue biology expand to involve systemic metabolism through alterations in endocrine functions of adipose tissue (via disturbed adipokine release), enhanced production of pro-inflammatory cytokines and excessive free fatty-acid release due to lipolysis. The deleterious action of some antiretroviral drugs is an important factor in eliciting these alterations in adipose tissue. However, HIV-1 infection-related events and HIV-1-encoded proteins also contribute directly to the complex development of HALS through effects on adipocyte biology, or indirectly through the promotion of local inflammation in adipose tissue. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:487 / 499
页数:13
相关论文
共 93 条
[1]   Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia, and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy [J].
Addy, CL ;
Gavrila, A ;
Tsiodras, S ;
Brodovicz, K ;
Karchmer, AW ;
Mantzoros, CS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2003, 88 (02) :627-636
[2]   Effects of transgenic expression of HIV-1 Vpr on lipid and energy metabolism in mice [J].
Balasubramanyam, Ashok ;
Mersmann, Harry ;
Jahoor, Farook ;
Phillips, Terry M. ;
Sekhar, Rajagopal V. ;
Schubert, Ulrich ;
Brar, Baljinder ;
Iyer, Dinakar ;
Smith, E. O'Brian ;
Takahashi, Hideko ;
Lu, Huiyan ;
Anderson, Peter ;
Kino, Tomoshige ;
Henklein, Peter ;
Kopp, Jeffrey B. .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2007, 292 (01) :E40-E48
[3]   Association between altered expression of adipogenic factor SREBP1 in lipoatrophic adipose tissue from HIV-1-infected patients and abnormal adipocyte differentiation and insulin resistance [J].
Bastard, JP ;
Caron, M ;
Vidal, H ;
Jan, V ;
Auclair, M ;
Vigouroux, C ;
Luboinski, J ;
Laville, M ;
Malachi, M ;
Girard, PM ;
Rozenbaum, W ;
Levan, P ;
Capeau, J .
LANCET, 2002, 359 (9311) :1026-1031
[4]   Nelfinavir-induced insulin resistance is associated with impaired plasma membrane recruitment of the PI 3-kinase effectors Akt/PKB and PKC-ζ [J].
Ben-Romano, R ;
Rudich, A ;
Tirosh, A ;
Potashnik, R ;
Sasaoka, T ;
Riesenberg, K ;
Schlaeffer, F ;
Bashan, N .
DIABETOLOGIA, 2004, 47 (06) :1107-1117
[5]   HIV protease inhibitors activate the adipocyte renin angiotensin system [J].
Boccara, Franck ;
Auclair, Martine ;
Cohen, Ariel ;
Lefevre, Chloe ;
Prot, Mathieu ;
Bastard, Jean-Philippe ;
Capeau, Jacqueline ;
Caron-Debarle, Martine .
ANTIVIRAL THERAPY, 2010, 15 (03) :363-375
[6]   Adipocyte differentiation, mitochondrial gene expression and fat distribution: differences between zidovudine and tenofovir after 6 months [J].
Boothby, Meg ;
McGee, Kirsty C. ;
Tomlinson, Jeremy W. ;
Gathercole, Laura L. ;
McTernan, Philip G. ;
Shojaee-Moradie, Fariba ;
Umpleby, A. Margot ;
Nightingale, Peter ;
Shahmanesh, Mohsen .
ANTIVIRAL THERAPY, 2009, 14 (08) :1089-1100
[7]   Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy [J].
Brinkman, K ;
Smeitink, JA ;
Romijn, JA ;
Reiss, P .
LANCET, 1999, 354 (9184) :1112-1115
[8]   Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence [J].
Caron, M. ;
Auclair, M. ;
Donadille, B. ;
Bereziat, V. ;
Guerci, B. ;
Laville, M. ;
Narbonne, H. ;
Bodemer, C. ;
Lascols, O. ;
Capeau, J. ;
Vigouroux, C. .
CELL DEATH AND DIFFERENTIATION, 2007, 14 (10) :1759-1767
[9]   The HIV-1 nucleoside reverse transcriptase inhibitors stavudine and zidovudine alter adipocyte functions in vitro [J].
Caron, M ;
Auclair, M ;
Lagathu, C ;
Lombès, A ;
Walker, UA ;
Kornprobst, M ;
Capeau, J .
AIDS, 2004, 18 (16) :2127-2136
[10]  
Caron M, 2008, ANTIVIR THER, V13, P27