Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/55778
Type: Artigo
Title: Blockade of IRS1 in isolated rat pancreatic islets improves glucose-induced insulin secretion
Title Alternative: 
Author: Araujo, E.P.
Amaral, M.E.C.
Souza, C.T.
Bordin, S.
Ferreira, F.
Saad, M.J.A.
Boschero, A.C.
Magalhaes, E.C.
Velloso, L.A.
Abstract: Several neural, hormonal and biochemical inputs actively participate in the balance of insulin secretion induced by blood glucose fluctuations. The exact role of insulin as an autocrine and paracrine participant in the control of its own secretion remains to be determined, mostly due to insufficient knowledge about the molecular phenomena that govern insulin signaling in pancreatic islets. In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. These data reinforce the inhibitory role of insulin upon its own secretion in isolated, undisrupted pancreatic islets. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved
metadata.dc.description.abstractalternative: 
Subject: Insulina
Receptor de insulina
Glucagon
Somatostatina
Country: Reino Unido
Editor: John Wiley & Sons
Citation: Febs Letters. Elsevier Science Bv, v. 531, n. 3, n. 437, n. 442, 2002.
Rights: fechado
Identifier DOI: 10.1016/S0014-5793(02)03580-9
Address: https://febs.onlinelibrary.wiley.com/doi/full/10.1016/S0014-5793%2802%2903580-9
Date Issue: 2002
Appears in Collections:IB - Artigos e Outros Documentos
FCM - Artigos e Outros Documentos

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