T cell-mediated hepatic inflammation modulates adiponectin levels in mice:: role of tumor necrosis factor α

被引：12
作者：
Morris, AM
Sennello, JA
Fayad, RA
Eckel, RH
Dinarello, CA
Fantuzzi, G
机构：
[1] Univ Colorado, Hlth Sci Ctr, Div Endocrinol, Denver, CO 80262 USA
[2] Univ Colorado, Hlth Sci Ctr, Div Infect Dis, Denver, CO 80262 USA
来源：
METABOLISM-CLINICAL AND EXPERIMENTAL | 2006年 / 55卷 / 04期
关键词：
D O I：
10.1016/j.metabol.2005.11.008
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Experimental T cell-mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor alpha (TNF-alpha). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-alpha reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-alpha is a critical mediator of adipose-tissue-derived adiponectin in vivo. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码：555 / 559
页数：5
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