PTPase (Protein Tyrosine Phosphatases) catalyze the dephosphorylation of insulin receptor and its substrates, leading to attenuation of insulin action. A number of PTPases have been implicated as the negative regulator of insulin signaling. Among them, the intracellular PTPase, PTP1B, has been shown to function as the insulin receptor phosphatase. PTEN (Phosphatase and Tensin Homolog Deleted On Chromosome-10) negatively regulates insulin signaling. SHIP2 (SH2-containing Inositol Phosphatase-2) is another negative regulator of insulin signaling and such negative regulation depends on its 5'-phopshatase activity. Overexpression of SHIP2 protein decreases Insulin-dependent PIP3 production as well as insulin-stimulated Akt activation, GSK3 inactivation, and glycogen synthetase activation. Insulin increases glucose uptake in muscle and fat, and inhibits hepatic glucose production, thus serving as the primary regulator of blood glucose concentration. Insulin also stimulates cell growth and differentiation, and promotes the storage of substrates in fat, liver and muscle by stimulating lipogenesis, glycogen and protein synthesis, and inhibiting lipolysis, glycogenolysis and protein breakdown. Insulin resistance or deficiency results in profound dysregulation of these processes, and produces elevations in fasting and postprandial glucose and lipid levels.
Many hormones and their structural and functional analogs are used as medication . The most commonly prescribed hormones are estrogens and progestogens (as methods of hormonal contraception and as HRT ),  thyroxine (as levothyroxine , for hypothyroidism ) and steroids (for autoimmune diseases and several respiratory disorders ). Insulin is used by many diabetics . Local preparations for use in otolaryngology often contain pharmacologic equivalents of adrenaline , while steroid and vitamin D creams are used extensively in dermatological practice.