Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/102491
Type: Artigo de periódico
Title: Peroxisome Proliferator-activated Receptor γ Coactivator-1-dependent Uncoupling Protein-2 Expression In Pancreatic Islets Of Rats: A Novel Pathway For Neural Control Of Insulin Secretion
Author: De Souza C.T.
Gasparetti A.L.
Pereira-da-Silva M.
Araujo E.P.
Carvalheira J.B.
Saad M.J.A.
Boschero A.C.
Carneiro E.M.
Velloso L.A.
Abstract: Aims/hypothesis. Sympathetic inputs inhibit insulin secretion through α2-adrenergic receptors coupled with Gi protein. High adrenergic tonus generated by exposure of homeothermic animals to cold reduces insulin secretion. In this study we evaluate the participation of UCP-2 in cold-induced regulation of insulin secretion. Methods. Static insulin secretion studies, western blotting and immunohistochemistry were used in this investigation. Results. Exposure of rats to cold during 8 days promoted 60% (n=15, p<0.05) reduction of basal serum insulin levels concentration accompanied by reduction of the area under insulin curve during i.p. GTT (50%, n=15, p<0.05). Isolated islets from cold-exposed rats secreted 57% (n=6, p<0.05) less insulin following a glucose challenge. Previous sympathectomy, partially prevented the effect of cold exposure upon insulin secretion. Islets isolated from cold-exposed rats expressed 51% (n=6, p<0.5) more UCP-2 than islets from control rats, while the inhibition of UCP-2 expression by antisense oligonucleotide treatment partially restored insulin secretion of islets obtained from cold-exposed rats. Cold exposure also induced an increase of 69% (n=6, p<0.05) in PGC-1 protein content in pancreatic islets. Inhibition of islet PGC-1 expression by antisense oligonucleotide abrogated cold-induced UCP-2 expression and partially restored insulin secretion in islets exposed to cold. Conclusion/interpreatation. Our data indicate that sympathetic tonus generated by exposure of rats to cold induces the expression of PGC-1, which participates in the control of UCP-2 expression in pancreatic islets. Increased UCP-2 expression under these conditions could reduce the beta-cell ATP/ADP ratio and negatively regulate insulin secretion.
Editor: 
Rights: fechado
Identifier DOI: 10.1007/s00125-003-1222-5
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-0345548705&partnerID=40&md5=e9f5be11f50bca6b1c76f00394e53aa5
Date Issue: 2003
Appears in Collections:Unicamp - Artigos e Outros Documentos

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