Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/340433
Type: Artigo
Title: The 17-beta-estradiol improves insulin sensitivity in a rapid estrogen receptor alpha-dependent manner in an animal model of malnourishment
Author: Garcia-Arevalo, Marta
Lorza-Gil, Estela
Leite, Nayara
Brunetto, Sergio
Boschero, Antonio Carlos
Carneiro, Everardo Magalhaes
Abstract: Protein restriction causes metabolic programming to maintain glucose homeostasis in rodents. They develop increased insulin sensitivity in peripheral tissues and reduced insulin secretion by pancreatic beta cells. Estradiol (E2) is a steroid hormone involved in the control of energy balance and glucose homeostasis. Here, we assessed the role of estrogen receptors (ERs) on glucose homeostasis in malnourished mice and the effect of E2 on insulin signaling. Methods: Post-weaned Swiss male mice were fed a low-protein (LP, 6%) or chow diet (control, 14%) for 8 weeks. The malnourished phenotype in LP mice was confirmed by different physiological parameters. Hypersensitivity to insulin was demonstrated by a higher glucose infusion in the LP group compared with the control by euglycemic-hyperinsulinemic clamp. Results: The administration of 10 mu g/kg E2 during the clamp induced a significant increase in the glucose infusion rate in the LP group compared with the control, indicating enhanced insulin sensitivity in LP mice. In addition, E2 administration increased glucose uptake by peripheral tissues. These effects were blunted in mice treated with general ER antagonists (ICI 182,780 and MPP). However, PHTTP failed to interfere with the E2 effect on insulin sensitivity. In the estradiol LP-treated mice, the activity of the insulin pathway was augmented, as demonstrated by higher AKT phosphorylation and glucose uptake by the skeletal muscle. Conclusion: Thus, we show an acute effect of E2 on insulin signaling in the skeletal muscle of protein-restricted mice. It is mediated by ER alpha, which interacts directly with phosphatidylinositol 3-kinase (PI3K), increasing the phosphorylation of AKT and consequently, glucose uptake in muscle
Subject: Resistência à insulina
Country: Canadá
Editor: Elmer Press
Rights: Aberto
Identifier DOI: 10.14740/jem612
Address: https://www.jofem.org/index.php/jofem/article/view/612
Date Issue: 2019
Appears in Collections:IB - Artigos e Outros Documentos
CEB - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000489755600004.pdf2.74 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.