Interaction between Leptin and InsulinSignaling Pathways Differentially AffectsJAK-STAT and PI 3-Kinase-Mediated Signalingin Rat Liver

Verfasser / Beitragende:
[J.B.C. Carvalheira, E.B. Ribeiro, F. Folli, L.A. Velloso, M.J.A. Saad]
Ort, Verlag, Jahr:
2003
Enthalten in:
Biological Chemistry, 384/1(2003-01-27), 151-159
Format:
Artikel (online)
ID: 378849662
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245 0 0 |a Interaction between Leptin and InsulinSignaling Pathways Differentially AffectsJAK-STAT and PI 3-Kinase-Mediated Signalingin Rat Liver  |h [Elektronische Daten]  |c [J.B.C. Carvalheira, E.B. Ribeiro, F. Folli, L.A. Velloso, M.J.A. Saad] 
520 3 |a Chronic leptin treatment markedly enhances the effect of insulin on hepatic glucose production unproportionally with respect to body weight loss and increased insulin sensitivity. In the present study the cross-talk between insulin and leptin was evaluated in rat liver. Upon stimulation of JAK2 tyrosine phosphorylation, leptin induced JAK2 co-immunoprecipitation with STAT3, STAT5b, IRS-1 and IRS-2. This phenomenon parallels the leptininduced tyrosine phosphorylation of STAT3, STAT5b, IRS-1 and IRS-2. Acutely injected insulin stimulated a mild increase in tyrosine phosphorylation of JAK2, STAT3 and STAT5b. Leptin was less effective than insulin in stimulating IRS phosphorylation and their association with PI 3-kinase. Simultaneous treatment with both hormones yielded no change in maximal phosphorylation of STAT3, IRS-1, IRS-2 and Akt, but led to a marked increase in tyrosine phosphorylation of JAK2 and STAT5b when compared with isolated administration of insulin or leptin. This indicates that there is a positive crosstalk between insulin and leptin signaling pathways at the level of JAK2 and STAT5b in rat liver. 
540 |a Copyright © 2003 by Walter de Gruyter GmbH & Co. KG 
690 7 |a Biochemistry  |2 nationallicence 
690 7 |a Molecular biology  |2 nationallicence 
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700 1 |a Ribeiro  |D E.B.  |4 aut 
700 1 |a Folli  |D F.  |4 aut 
700 1 |a Velloso  |D L.A.  |4 aut 
700 1 |a Saad  |D M.J.A.  |4 aut 
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