Environmental chemical tributyltin augments adipocyte differentiation

被引:93
作者
Inadera, H [1 ]
Shimomura, A [1 ]
机构
[1] Toyama Med & Pharmaceut Univ, Fac Med, Dept Publ Hlth, Toyama 9300194, Japan
关键词
tributyltin; 3T3-L1; cell; adipocyte; sex-steroid;
D O I
10.1016/j.toxlet.2005.05.015
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Scientific attention has been drawn to environmental factors that affect obesity and type II diabetes. Previously, acute organotin toxicosis was reported to induce hyperglycernia without morphological abnormalities in islet tissue, suggesting that these compounds have a direct effect on adipose tissue. Therefore, we investigated the effect of tributyltin (TBT) on adipocyte differentiation. When confluent 3T3-L1 cells were incubated with TBT for 2 days in the presence or absence of isobutyl methylxanthine, dexamethasone and insulin (MDI), the lipid accumulation in adipocytes was greatly enhanced. These morphological changes induced by TBT were accompanied by the expression of a differentiation marker for adipocytes in a dose-dependent manner. Co-treatment with the peroxisome proliferator-activated receptor (PPAR)gamma antagonist GW9662 did not inhibit the effect of TBT, suggesting that the observed effect of TBT may not be PPAR gamma-dependent. Although TBT was reported to exert androgenic effects and inhibit the activity of aromatase, treatments with dihydrotestosterone or 17 beta-estradiol did not influence the aP2 expression in 3T3-L1 cells, suggesting that the TBT effect does not occur via sex-steroids. These findings indicate that TBT may be one of the environmental chemicals that lead to excessive accumulation of adipose tissue, which can result in obesity. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:226 / 234
页数:9
相关论文
共 55 条
[31]   Serum dioxin level in relation to diabetes mellitus among Air Force Veterans with background levels of exposure [J].
Longnecker, MP ;
Michalek, JE .
EPIDEMIOLOGY, 2000, 11 (01) :44-48
[32]   TRANSCRIPTIONAL REGULATION OF GENE-EXPRESSION DURING ADIPOCYTE DIFFERENTIATION [J].
MACDOUGALD, OA ;
LANE, MD .
ANNUAL REVIEW OF BIOCHEMISTRY, 1995, 64 :345-373
[33]   THE RXR HETERODIMERS AND ORPHAN RECEPTORS [J].
MANGELSDORF, DJ ;
EVANS, RM .
CELL, 1995, 83 (06) :841-850
[34]  
Masuno H, 2002, J LIPID RES, V43, P676
[35]   SPECIES-DIFFERENCE IN SENSITIVITY TO THE DIABETOGENIC ACTION OF TRIPHENYLTIN HYDROXIDE [J].
MATSUI, H ;
WADA, O ;
MANABE, S ;
USHIJIMA, Y ;
FUJIKURA, T .
EXPERIENTIA, 1984, 40 (04) :377-378
[36]   Retinoid receptors in transcriptional regulation [J].
Minucci, S ;
Ozato, K .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 1996, 6 (05) :567-574
[37]   Involvement of the retinoid X receptor in the development of imposex caused by organotins in gastropods [J].
Nishikawa, J ;
Mamiya, S ;
Kanayama, T ;
Nishikawa, T ;
Shiraishi, F ;
Horiguchi, T .
ENVIRONMENTAL SCIENCE & TECHNOLOGY, 2004, 38 (23) :6271-6276
[38]   CHELATION OF INTRACELLULAR CALCIUM BLOCKS INSULIN ACTION IN THE ADIPOCYTE [J].
PERSHADSINGH, HA ;
SHADE, DL ;
DELFERT, DM ;
MCDONALD, JM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (04) :1025-1029
[39]   Adipocytokines and insulin resistance [J].
Pittas, AG ;
Joseph, NA ;
Greenberg, AS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (02) :447-452
[40]  
Rosen ED, 2000, GENE DEV, V14, P1293