Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 382, Issue 4, Pages 646-650Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.02.154
Keywords
Estrogen; ICI 182,780; Skeletal muscle; AS160; Insulin signaling
Categories
Funding
- United States Department of Agriculture, Tufts Medical Center, NIDDK, American Diabetes Association [5819507707, T32DK062032, 50647]
- National Institutes of Health [R01 AR45670]
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Post-menopausal women exhibit decreases in circulating estrogen levels and whole body insulin sensitivity, suggesting that estrogen regulates skeletal muscle glucose disposal. Thus, we assessed whether estrogen stimulates glucose uptake or enhances insulin sensitivity in skeletal muscle. Ex vivo muscle Stimulation with 17 beta-estradiol (10 nM) resulted in a rapid (<= 10 min) increase in the phosphorylation of Akt, AMP-activated protein kinase (AMPK), and TBC1D1/4, key signaling Proteins that regulate glucose uptake in muscle. Treatment with the estrogen receptor antagonist, ICI 182,780, only partly inhibited signaling, suggesting both an estrogen receptor-dependent and independent mechanism of estradiol action. 17 beta-Estradiol did not stimulate ex vivo muscle [H-3]-2-deoxyglucose Uptake or enhance insulin-induced glucose Uptake, demonstrating discordance between the estradiol-induced stimulation of signaling proteins and muscle glucose uptake. This study is the first to demonstrate that estradiol stimulates Akt, AMPK, and TBC1D1/4 in intact skeletal muscle, but surprisingly, estradiol does not stimulate muscle glucose uptake. (C) 2009 Elsevier Inc. All rights reserved.
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