After 1990 Cicirelli and other first proposed PTP-1B and insulin signal transduction related to the Xenopus oocyte microinjection of PTP-1B, hindered the insulin peptide phosphorylation of S6 and delayed insulin promote oocyte maturation. This study marks a milestone reveals the PTP-1B negative regulatory role in insulin signal transduction. PTP1B specific hydrolysis of an aromatic acid, such as phosphotyrosine (pTyr) residues of the enzyme on the phosphate through a tyrosine residue or a substrate for the insulin receptor on the dephosphorylation of the insulin signal transduction guide were negative regulator, tissue cells overexpressing PTP-1B will reduce PTK activity, so that the insulin receptor can not be combined with insulin, thereby causing insulin resistance, ultimately leading to type 2 diabetes.
Elchebly such as the use of gene knockout technology, PTP-1B knockout mice were insulin resistance and sensitivity studies, a clear relationship between PTP-1B and type 2 diabetes and obesity diseases. The study found that in the PTP-1B knockout mice skeletal muscle and liver, insulin receptor autophosphorylation increased insulin sensitivity increase, and resistance to weight gain. The study defined the PTP-1B is the treatment of type 2 diabetes and obesity targets, indicating that PTP-1B inhibitors by improving insulin sensitivity, which can effectively treat type 2 diabetes and obesity.
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