Interaction between Leptin and InsulinSignaling Pathways Differentially AffectsJAK-STAT and PI 3-Kinase-Mediated Signalingin Rat Liver
Gespeichert in:
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)
Online Zugang:
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| 024 | 7 | 0 | |a 10.1515/BC.2003.016 |2 doi |
| 035 | |a (NATIONALLICENCE)gruyter-10.1515/BC.2003.016 | ||
| 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 | |
| 690 | 7 | |a Cellular biology |2 nationallicence | |
| 700 | 1 | |a Carvalheira |D J.B.C. |4 aut | |
| 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 | |
| 773 | 0 | |t Biological Chemistry |d Walter de Gruyter |g 384/1(2003-01-27), 151-159 |x 1431-6730 |q 384:1<151 |1 2003 |2 384 |o bchm | |
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| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Carvalheira |D J.B.C. |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Ribeiro |D E.B. |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Folli |D F. |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Velloso |D L.A. |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Saad |D M.J.A. |4 aut | ||
| 950 | |B NATIONALLICENCE |P 773 |E 0- |t Biological Chemistry |d Walter de Gruyter |g 384/1(2003-01-27), 151-159 |x 1431-6730 |q 384:1<151 |1 2003 |2 384 |o bchm | ||
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