期刊
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 116, 期 3-5, 页码 160-170出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2009.05.010
关键词
Insulin resistance; 17 beta-Estradiol; Glut4; p85 alpha; IRS-1; Pregnancy
资金
- Fondo de Investigaciones Sanitarias, Spain [P1020324]
- Oviedo University [UNOV-06-MB-516, UNOV-07-MB06-516]
Maternal metabolic adaptations are essential to ensure proper fetal development. According to changes in insulin sensitivity, pregnancy can be divided into two periods: early pregnancy, characterized by an increase in maternal insulin sensitivity, and late pregnancy, in which there is a significant increase in insulin resistance. The aims of the present work were two-fold: firstly, the molecular mechanisms associated with the development of pregnancy-related insulin resistance in peripheral tissues, mainly retroperitoneal adipose tissue and skeletal muscle, were studied in pregnant rats at 6, 11, and 16 days gestation. Secondly, the role of 17 beta-estradiol in this process was elucidated in an animal model consisting of ovariectomized rats treated with 17 beta-estradiol to mimic plasma gestational levels. The results support the conclusion that retroperitoneal adipose tissue plays a pivotal role in the decrease in insulin sensitivity during pregnancy, through a mechanism that involves p85 alpha redistribution to the insulin receptor and impairment of Glut4 translocation to the plasma membrane. Treatment with 17 beta-estradiol did not reproduce the molecular adaptations that occur during pregnancy, suggesting that other hormonal factors presents in gestation but absent in our experimental model are responsible for p85 alpha redistribution to the insulin receptor. (C) 2009 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据