Volume 22, No 11, Nov 2012

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 22 Issue 11, November 2012: 1530-1532

RESEARCH HIGHLIGHTS

InsP3R-Ca2+ signaling takes center stage in the hormonal regulation of hepatic gluconeogenesis

Michihiro Matsumoto

Department of Molecular Metabolic Regulation, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo 162-8655, Japan Correspondence: Michihiro Matsumoto,(mmatsumoto@ri.ncgm.go.jp)

During fasting, dephosphorylation-dependent activation of the CREB coactivator CRTC2 by glucagon is crucial for activation of the hepatic gluconeogenic program, but the molecular mechanism by which hormones regulate CRTC2 activation remains unclear. A recent report in Nature showed that PKA-dependent phosphorylation of the inositol-1,4,5-trisphosphate receptor (InsP3R) induces Ca2+ mobilization, leading to increase in the phosphatase activity of calcineurin and the subsequent dephosphorylation of CRTC2, thereby resulting in the induction of gluconeogenic gene expression. It also showed that insulin-dependent phosphorylation of InsP3R by Akt inhibits Ca2+ mobilization and CRTC2 dephosphorylation, resulting in the suppression of gluconeogenesis.

Cell Research (2012) 22:1530-1532. doi:10.1038/cr.2012.95; published online 19 June 2012

FULL TEXT | PDF

Browse 2145