Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/60297
Type: Artigo de periódico
Title: Insulin modulates leptin-induced STAT3 activation in rat hypothalamus
Author: Carvalheira, JBC
Siloto, RMP
Ignacchitti, I
Brenelli, SL
Carvalho, CRO
Leite, A
Velloso, LA
Gontijo, JAR
Saad, MJA
Abstract: Insulin and leptin have overlapping effects in the control of energy homeostasis, but the molecular basis of this synergism is unknown, Insulin signals through a receptor tyrosine kinase that phosphorylates and activates the docking proteins IRSs (insulin receptor substrates), whereas the leptin receptor and its associated protein tyrosine kinase JAK2 (Janus kinase 2) mediate phosphorylation and activation of the transcription factor STAT3 (signal transducer and activator of transcription). Here, we present evidence for the integration of leptin and insulin signals in the hypothalamus. Insulin induced JAK2 tyrosine phosphorylation, leptin receptor phosphorylation which, in the presence of leptin, augmented the interaction between STAT3 and this receptor. Insulin also increased the leptin-induced phosphorylation of STAT3 and its activation. These results indicate that insulin modulates the leptin signal transduction pathway, and may provide a molecular basis for the coordinated effects of insulin and leptin in feeding behavior and weight control. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
Subject: leptin
insulin
tyrosine phosphorylation
Janus kinase 2
signal transducer and activator of transcription
long form of the leptin receptor
Country: Holanda
Editor: Elsevier Science Bv
Rights: fechado
Identifier DOI: 10.1016/S0014-5793(01)02591-1
Date Issue: 2001
Appears in Collections:Unicamp - Artigos e Outros Documentos

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