While prolonged GCGR activation is typically associated with elevated blood glucose levels and impaired glucose tolerance, short-term stimulation enhances glucose utilization and insulin responsiveness through hepatic RICTOR/mTORC2 and AKT signaling.145 These findings suggest that mTORC2 plays a supportive role in glucose metabolism upon GPCR activation and that this role may be functionally distinct from classical insulin/PI3K/AKT signaling. This evidence concerns the gene AKT1 and Impaired glucose tolerance.