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

FEBS letters (2012-12-25)
Delia Zafra, Laura Nocito, Jorge Domínguez, Joan J Guinovart
RÉSUMÉ

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.

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Sigma-Aldrich
Sodium tungstate dihydrate, ACS reagent, ≥99%
Sigma-Aldrich
Sodium tungstate dihydrate, BioUltra, ≥99.0% (T)
Sigma-Aldrich
Sodium tungstate dihydrate, 99.995% trace metals basis