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Sodium tungstate activates glycogen synthesis through a non‐canonical mechanism involving G‐proteins
Author(s) -
Zafra Delia,
Nocito Laura,
Domínguez Jorge,
Guinovart Joan J.
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.11.034
Subject(s) - glycogen synthase , glycogen , tungstate , chemistry , mapk/erk pathway , sodium tungstate , microbiology and biotechnology , signal transduction , protein kinase a , biochemistry , gsk 3 , mechanism of action , receptor , phosphorylation , biology , organic chemistry , tungsten , in vitro
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.