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). 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.
 The Insulin Receptor and Its Cellular Targets. Y. Kido, J. Nakae, D. Accili. J. Clin.Endocrin. Met. 2001, 86, 972-979.