Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 295, Issue 1-2, Pages 24-31Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.07.008
Keywords
17 Beta-estradiol; ERalpha; ERbeta; GLUT4 expression; Skeletal muscle; L6 cell; Gestational diabetes; Insulin resistance
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Funding
- Brazil's Ministry of Education
- State of Sao Paulo Research Foundation [02/13534-9, 02/07384-4]
- [CAPES/PDEE-BEX0145/05-0]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [02/07384-4] Funding Source: FAPESP
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Pregnancy is accompanied by hyperestrogenism, however, the role of estrogens in the gestational-induced insulin resistance is unknown. Skeletal muscle plays a fundamental role in this resistance, where GLUT4 regulates glucose uptake. We investigated: (1) effects of oophorectomy and estradiol (E2) on insulin sensitivity and GLUT4 expression. E2 (similar to 200 nM) for 7 days decreased sensitivity, reducing similar to 30% GLUT4 mRNA and protein (P< 0.05) and plasma membrane expression in muscle; (2) the expression of ER alpha and ER beta in L6 myotubes, showing that both coexpress in the same nucleus; (3) effects of E2 on GLUT4 in L6, showing a time- and dose-dependent response. High concentration (100 nM) for 6 days reduced similar to 25% GLUT4 mRNA and protein (P < 0.05). Concluding, E2 regulates GLUT4 in muscle, and at high concentrations, such as in pregnancy, reduces GLUT4 expression and, in vivo, decreases insulin sensitivity. Thus, hyperestrogenism may be involved in the pregnancy-induced insulin resistance and/or gestational diabetes. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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