AKT1 and diabetes mellitus: Sevoflurane postconditioning was abolished by chemically induced diabetes in a rat model and this detrimental effect involved the impairment of phosphorylation of glycogen synthase kinase 3-beta (GSK-3β) and its upstream pathways, such as PI3 kinase/Akt and extracellular signal regulated kinases (ERK) in diabetes [89].