Glucose homeostasis is regulated by hormones and cellular energy status. Elevations of blood glucose during feeding stimulate insulin release from pancreatic -cells through a glucose sensing pathway. Feeding also stimulates release of gut hormones such as glucagon-like peptide-1 (GLP-1), which further induces insulin release, inhibits glucagon release and promotes -cell viability. CREB-dependent transcription likely plays a role in both glucose sensing and GLP-1 signaling . The protein Torc2 (transducer of regulated CREB activity 2) functions as a CREB co-activator and is implicated in mediating the effects of these two pathways . In quiescent cells, Torc2 is phosphorylated at Ser171 and becomes sequestered in the cytoplasm via an interaction with 14-3-3 proteins. Glucose and gut hormones lead to the dephosphorylation of Torc2 and its dissociation from 14-3-3 proteins. Dephosphorylated Torc2 enters the nucleus to promote CREB-dependent transcription. Synonyms: TORC2, TORC-2, CRTC2