Author(s): Zafra D, Nocito L, Domnguez J, Guinovart JJ
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Abstract 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.
This article was published in FEBS Lett
and referenced in Journal of Clinical & Cellular Immunology