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This Article Full Text Full Text (PDF) All Versions of this Article: 297/1/E124    most recent 00189.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Barros, R. P. A. Articles by Gustafsson, J.-A. PubMed PubMed Citation Articles by Barros, R. P. A. Articles by Gustafsson, J.-A.

Participation of ER and ERβ in glucose homeostasis in skeletal muscle and white adipose tissue

¹Department of Biosciences and Nutrition, Karolinska Institutet, Novum, Sweden; and ²Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas

Submitted 23 March 2009 ; accepted in final form 9 April 2009

Glucose uptake and homeostasis are regulated mainly by skeletal muscle (SM), white adipose tissue (WAT), pancreas, and the liver. Participation of estradiol in this regulation is still under intense investigation. We have demonstrated that, in SM of male mice, expression of the insulin-regulated glucose transporter (GLUT)4 is reduced by estrogen receptor (ER)β agonists. In the present study, to investigate the relative contributions of ER and ERβ in glucose homeostasis, we examined the effects of tamoxifen (Tam) on GLUT4 expression in SM and WAT in wild-type (WT) and ER–/– mice. ERβ–/– mice were characterized by fasting hypoglycemia, increased levels of SM GLUT4, pancreatic islet hypertrophy, and a belated rise in plasma insulin in response to a glucose challenge. ER–/– mice, on the contrary, were hyperglycemic and glucose intolerant, and expression of SM GLUT4 was markedly lower than in WT mice. Tam had no effect on glucose tolerance or insulin sensitivity in WT mice. In ER–/– mice, Tam increased GLUT4 and improved insulin sensitivity. i.e., it behaved as an ERβ antagonist in SM but had no effect on WAT. In ERβ–/– mice, Tam did not affect GLUT4 in SM but acted as an ER antagonist in WAT, decreasing GLUT4. Thus, in the interplay between ER and ERβ, ERβ-mediated repression of GLUT4 predominates in SM but ER-mediated induction of GLUT4 predominates in WAT. This tissue-specific difference in dominance of one ER over the other is reflected in the ratio of the expression of the two receptors. ER predominates in WAT and ERβ in SM.

estrogen receptor-; estrogen receptor-β; glucose transporter 4; tamoxifen

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