Sodium tungstate activates glycogen synthesis through a non-canonical mechanism involving G-proteins.

Delia Zafra, Laura Nocito, Jorge Domínguez, Joan J Guinovart

Institute for Research in Biomedicine (IRB Barcelona) and Department of Biochemistry and Molecular Biology, University of Barcelona, and CIBER de Diabetes y Enfermedades Metabólicas (CIBERDEM), Baldiri Reixac 10-12, E-08028 Barcelona, Spain.

FEBS letters 2013 Jan 31

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Tungstate treatment ameliorates experimental diabetes by increasing liver glycogen deposition through an as yet unidentified mechanism. The signalling mechanism of tungstate was studied in CHOIR cells and primary cultured hepatocytes. This compound exerted its pro-glycogenic effects through a new G-protein-dependent and Tyr-Kinase Receptor-independent mechanism. Chemical or genetic disruption of G-protein signalling prevented the activation of the Ras/ERK cascade and the downstream induction of glycogen synthesis caused by tungstate. Thus, these findings unveil a novel non-canonical signalling pathway that leads to the activation of glycogen synthesis and that could be exploited as an approach to treat diabetes. Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Citation

Delia Zafra, Laura Nocito, Jorge Domínguez, Joan J Guinovart. Sodium tungstate activates glycogen synthesis through a non-canonical mechanism involving G-proteins. FEBS letters. 2013 Jan 31;587(3):291-6