Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/80058
Type: Artigo
Title: Regulation of insulin-stimulated tyrosine phosphorylation of Shc and Shc/Grb2 association in liver, muscle, and adipose tissue of epinephrine- and streptozotocin-treated rats
Author: Paez-Espinosa, V.
Saad, M.J.A.
Velloso, L.A.
Rocha, E.M.
Abstract: Shc protein phosphorylation has been extensively characterized as the initial step that activates a complex mitogenic pathway through its association with Grh2. In the present study, we investigated the adrenergic control of insulin-induced She phosphorylation and Shc-Grb2 association, and the modulating effect of streptozotocin-induced diabetes mellitus on She phosphorylation and Shc/Grb2 association. Acute treatment with epinephrine, which leads to a normoglycemic insulin-resistant state, does not affect insulin-induced She tyrosine phosphorylation or Shc-Grb2 association in liver, muscle, or fat. By contrast, a significant increase in insulin-induced She phosphorylation is observed in liver and muscle of rats treated with streptozotocin. The association of Shc/Grb2 is also increased in both tissues following insulin treatment, These data suggest that while epinephrine preserves the insulin/induced phosphorylation of She and the mitogenic pathway stimulated by Shc-Grb2 association, treatment with streptozotocin leads to a tissue-specific increase in the activity of the initial step that ultimately results in the activation of the Shc/Grb2 mitogenic pathway
Subject: Estreptozocina
Diabetes mellitus
Country: Alemanha
Editor: Springer
Citation: Endocrine. Humana Press Inc, v. 14, n. 3, n. 295, n. 302, 2001.
Rights: fechado
Identifier DOI: 10.1385/ENDO:14:3:295
Address: https://link.springer.com/article/10.1385/ENDO:14:3:295
Date Issue: 2001
Appears in Collections:FCM - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
169301400003.pdf417.29 kBAdobe PDFView/Open


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