Regulation of adiponectin receptor expression in human liver and a hepatocyte cell line

被引：45

作者：

Shimizu, Akiko

Takamura, Toshinari ^{[1
]}

Matsuzawa, Naoto

Nakamura, Seiji

Nabemoto, Satoko

Takeshita, Yurnie

Misu, Hirofumi

Kurita, Seiichiro

Sakurai, Masaru

Yokoyama, Masayoshi

Zen, Yoh

Sasaki, Motoko

Nakanuma, Yasuni

Kaneko, Shuichi

机构：

[1] Kanazawa Univ, Dept Dis Control & Homeostasis, Grad Sch Med Sci, Kanazawa, Ishikawa 9208641, Japan

[2] Kanazawa Univ, Dept Human Pathol, Grad Sch Med Sci, Kanazawa, Ishikawa 9208641, Japan

来源：

METABOLISM-CLINICAL AND EXPERIMENTAL | 2007年 / 56卷 / 11期

关键词：

D O I：

10.1016/j.metabol.2007.06.013

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Nonalcoholic fatty liver disease (NAFLD) is closely associated with obesity. An adipocyte-derived hormone, adiponectin, may play a role in the pathophysiolo-gy of NAFLD through insulin-sensitizing and antifibrotic effects. We found that hepatic expression of adiponectin receptor AdipoR2, but not AdipoR1, was down-regulated in 14 patients with NAFLD compared with 7 patients with a normal liver (P <.05). To investigate the significance of the adiponectin system in obesity and NAFLD, we examined the regulation of AdipoR2 expression in a nonmalienant human hepatocyte cell line, the THLE-5b cells. Insulin down-regulated the levels of AdipoR2 messenger RNA (mRNA) and protein, whereas an adipocyrokine, turnor necrosis factor g., up-regulated them. A thiazolidinedione, pioglitazone, up-regulated the expression of AdipoR2 mRNA and protein in THLE-5b cells. The AdipoR2 mRNA level was decreased in fatty THLE-5b cells induced by coincubating with fatty acids. These findings suggest that down-regulation of AdipoR2 in the liver caused by hypermsulinernia and steatosis may play a role in the development of NAFLD. (C) 2007 Elsevier hic. All rights reserved.

引用

页码：1478 / 1485

页数：8

共 41 条

[21] Pioglitazone prevents hepatic steatosis, fibrosis, and enzyme-altered lesions in rat liver cirrhosis induced by a choline-deficient L-amino acid-defined diet [J].