Resistin mRNA levels are downregulated by estrogen in vivo and in vitro

被引：42

作者：

Huang, SW

Seow, KM

Ho, LT

Chien, Y

Chung, DY

Chang, CL

Lai, YH

Hwang, JL

Juan, CC ^{[1
]}

机构：

[1] Natl Yang Ming Univ, Inst Clin Med, Taipei 112, Taiwan

[2] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan

[3] Natl Yang Ming Univ, Inst Physiol, Taipei 112, Taiwan

[4] Shin Kong Wu Ho Su Mem Hosp, Dept Obstet & Gynecol, Taipei, Taiwan

[5] Dept Med Res & Educ, Taipei, Taiwan

[6] Taipei Vet Gen Hosp, Dept Internal Med, Taipei, Taiwan

[7] Fu Jen Catholic Univ, Sch Med, Taipei, Taiwan

[8] Taipei Med Univ, Dept Obstet & Gynecol, Taipei, Taiwan

[9] Shou Univ, E Da Hosp, Dept Obstet & Gynecol, Kaohsiung, Taiwan

来源：

FEBS LETTERS | 2005年 / 579卷 / 02期

关键词：

resistin; estrogen; adipocyte; ovariectomy;

D O I：

10.1016/j.febslet.2004.12.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Resistin, a hormone secreted by adipocytes, is suggested to be an important link between obesity and diabetes. The aim of this study was to evaluate the regulatory effect of estrogen on adipocyte resistin gene expression in ovariectomized (OVX) rats and in isolated rat adipocytes in vitro. Subcutaneous injection of estradiol benzoate reduced resistin mRNA levels in adipocytes isolated from the inguinal, parametrial, perirenal, retroperitoneal, or periovarian fat deposits of OVX rats, while an in vitro study showed that estradiol treatment decreased resistin mRNA levels in cultured rat periovarian fat adipocytes. Results of Western blotting analysis also showed that estrogen decreased adipose resistin contents in vivo and in vitro. These data suggest that estrogen is a pivotal negative regulator of resistin gene expression. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：449 / 454

页数：6

共 36 条

[1] Changes in glycemia by leptin administration or high-fat feeding in rodent models of obesity/type 2 diabetes suggest a link between resistin expression and control of glucose homeostasis [J].