PI 3 K / AKT pathway in modulating glucose homeostasis and its alteration in Diabetes

Introduction Type 2 diabetes mellitus (T2DM), a complex disease which is characterized by a mixture of impaired insulin action, insulin secretory deficiency and increased endogenous glucose production. With theIn exception of β-cell failure, the resistance of target tissues to insulin is the main contributing incident to the development of T2DM [1,2]. Despite feeding and fasting phase in non-diabetic individuals, blood sugar remains in a narrow fluctuation and tightly controlled through the balance between glucose uptake by the intestine, glucose synthesis by the liver and ultimately glucose absorption by the peripheral tissues. Insulin is the main regulator and key hormone of glucose balance. It increases glucose absorption in muscles and adipose, and decreases glucose synthesis in the liver. In addition, cell growth and differentiation is stimulated by this hormone, which promotes the lipogenesis, protein and glycogen synthesis, and inhibiting lipolysis, proteolysis and glycogenolysis. It has shown that insulin promotes glucose absorption in cells by stimulating the glucose transporter GLUT4 transcription and translocation from the intracellular part to the cell membrane.