Hepatic Glucose Sensing via the CREB Coactivator CRTC2

A study conducted by the Salk Institute for Biological Studies recently showed that O-glycosyl transferase triggers hepatic gluconeogenesis through the O-glycosylation of the transducer of regulated CREB 2 (cAMP response element-binding protein, also called TORC2 or CRTC2).

CRTC2 was O-glycosylated at sites that usually emit CRTC2 in the cytoplasm via a phosphorylation-dependent mechanism. The effect of glucose on glucneogenesis was blocked by the deglycosylating enzyme O-GlcNAcase. Expression of this enzyme decreases the level of O-glycosylated CRTC2. This shows how important the hexosamine biosynthetic pathway is in the formation of glucose intolerance. Chronic hyperglycemia has a share in the development of diabetes-associated sequelae. If the concentration of circulating glucose is elevated, the hexosamine biosynthetic pathway is activated and promotes the O-glycosylation of proteins by O-glycosyl transferase.

Related antibodies on antibodies-online.com:

CREB

CRTC2

TORC2

OGT

O-GlcNAc

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