Chronic 17β-estradiol treatment improves skeletal muscle insulin signaling pathway components in insulin resistance associated with aging

被引：48
|
作者：
Moreno, M. [1 ]
Ordonez, P. [1 ]
Alonso, A. [1 ]
Diaz, F. [1 ]
Tolivia, J. [2 ]
Gonzalez, C. [1 ]
机构：
[1] Univ Oviedo, Dept Funct Biol, Physiol Area, Oviedo, Spain
[2] Univ Oviedo, Dept Morphol & Cellular Biol, Oviedo, Spain
来源：
AGE | 2010年 / 32卷 / 01期
关键词：
Aging; Insulin resistance; 17; beta-estradiol; Glut4; Akt; p85; alpha; IRS-1; FEMALE RATS; RECEPTOR SUBSTRATE-1; PHOSPHATIDYLINOSITOL; 3-KINASE; REPLACEMENT THERAPY; DIABETES-MELLITUS; GLUCOSE; SENSITIVITY; ESTROGEN; MECHANISMS; SECRETION;
D O I：
10.1007/s11357-009-9095-2
中图分类号：
R592 [老年病学]; C [社会科学总论];
学科分类号：
03 ; 0303 ; 100203 ;
摘要：
Insulin resistance is a common feature of aging in both humans and rats. In the case of females, it seems to be related to loss of gonadal function, due mainly due to a decrease in plasma estrogen levels. Several causes have been postulated for this insulin resistance, among them changes in several steps of the insulin pathway. In view of these findings, the purpose of the present study was to examine the role of chronic 17 beta-estradiol treatment on insulin sensitivity during the aging process, and its effects on levels of the insulin-sensitive glucose transporter Glut4 (both total and plasma membrane localized), the interaction between p85 alpha subunit of PI3-k and IRS-1, Tyr- and Ser-612 phosphorylation of IRS-1 levels, and Ser-473 phosphorylation of Akt. The present findings indicate that 17 beta-estradiol treatment is able to minimize the deleterious effect of aging on insulin sensitivity, at least at the level of plasma membrane localized Glut4. Nevertheless further research is needed to determine this conclusively.
引用
收藏
页码：1 / 13
页数：13
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