The pleiotropic actions of insulin are mediated by a single receptor tyrosine kinase (RTK class II, Insulin receptor family). A generally accepted paradigm is that insulin receptors, acting through insulin receptor substrates (insulin, and Insulin-like growth factors (IGF) I and II), stimulate the lipid kinase activity of phosphatidylinositol 3-kinase (PI3K)[1]. The rapid rise in Tris-phosphorylated inositol (PIP3) that ensues triggers a cascade of PIP3-dependent serine/threonine kinases. Among the latter, Akt  and atypical protein kinase C isoforms are thought to be involved in insulin regulation of glucose transport and oxidation; glycogen, lipid, and protein synthesis; and modulation of gene expression. "Insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes.