Figure 2.

Mechanism of action of insulin in the endothelial cell. The interaction of insulin with its receptor results in autophosphorylation of tyrosine residues and heterophosphorylation of second messengers such as IRS-1, which phosphorylates PI3K, leading to the activation of a cascade of phosphorylation ending with expression of various physiological effects, like the production of endothelial NO. IRS-1: insulin receptor substrate 1, PI3K: phosphatidylinositol 3-kinase, PIP₂: phosphatidylinositol diphosphate, PIP₃: phosphatidylinositol triphosphate, PDK-1: dependent kinase PI3K, Akt: protein kinase B, GLUT-4: glucose transporter 4, and NO: nitric oxide.