Figure 2.

Schematic model for role of FoxO1 in hepatic gluconeogenesis. After cerebral stroke, activation of Akt pathway in liver is inhibited. Then the phosphorylation of hepatic FoxO1 is suppressed which further leads to the nuclear translocation and activation of FoxO1. Activation of FoxO1, resulting in upregulation of hepatic PEPCK, G6Pase, and FBP at the transcriptional level, facilitated hepatic gluconeogenesis and the consequences of hyperglycemia after stroke. The solid lines represent the pathway that occurs after stroke, and the dotted line represents the pathway suppressed after stroke.