Epicardial Fat: Physiological, Pathological, and Therapeutic Implications

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.