Susan Aiston

TL;DR: GK activators are potential antihyperglycemic agents for the treatment of type 2 diabetes through the stimulation of hepatic glucose metabolism by a mechanism independent of GKRP.

TL;DR: It is concluded that the primary action of leptin in hepatocytes is to enhance glycogen storage, which may be an important compensatory mechanism for the inhibition of insulin secretion.

TL;DR: It is concluded that the main regulatory function of Glc-6-Pase is to buffer the glucose 6-phosphate concentration, consistent with recent findings that hyperglycemia stimulates GK gene transcription.

TL;DR: It is confirmed that phosphorylase is a strong candidate target for controlling hyperglycemia in type 2 diabetes in both the absorptive and postabsorptive states and has a very high negative control coefficient on glycogen synthesis, regardless of whether it is determined by enzyme inactivation or overexpression.

TL;DR: It is concluded that a signalling pathway involving dephosphorylation of phosphorylase a leading to both activation and translocation of glycogen synthase is a critical component of the mechanism by which insulin stimulates hepatic glycogen synthesis.