NDLI: Interaction between Leptin and Insulin Signaling Pathways Differentially Affects JAK-STAT and PI 3-Kinase-Mediated Signaling in Rat Liver

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Interaction between Leptin and Insulin Signaling Pathways Differentially Affects JAK-STAT and PI 3-Kinase-Mediated Signaling in Rat Liver

Content Provider	Semantic Scholar
Author	Carvalheira, José Barreto Campello Ribeiro, Eliane Beraldi Folli, Franco Velloso, Licio A. Saad, Mário José Abdalla
Copyright Year	2003
Abstract	Abstract 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.
Starting Page	151
Ending Page	159
Page Count	9
File Format	PDF HTM / HTML
DOI	10.1515/BC.2003.016
PubMed reference number	12674509
Journal	Medline
Volume Number	384
Alternate Webpage(s)	https://air.unimi.it/retrieve/handle/2434/469411/823722/bc.2003.016.pdf
Alternate Webpage(s)	https://doi.org/10.1515/BC.2003.016
Journal	Biological chemistry
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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