Primary Research The Effect Of SOCS-3 Gene On Insulin Resistance In Porcine Adipocyte

Porcine is an ideal model of human disease, because porcine is remarkably similar to human biological, metabolic and genetic levels. Insulin resistance and leptin resistance are the character of type 2 diabetes. They induce metabolic disorganized. The adipocyte plays a critical role in energy balance. Adipocyte also has endocrinic function which can secrete many kinds of adipokines. Such as: Leptin, TNFα,IL6 and so on, which can regulate energy metabolism. SOCS-3 is one of the main members of the SOCS family. Many cytokines'signaling such as Leptin, Insulin and IGF-Ⅰwas regulated by SOCS-3 in adipocyte. It can induce insulin resistance and leptin resistance. In this study, we investigated the expression pattern of SOCS-3 mRNA in primary culture adipocyte, which treated with insulin, insulin and glucose and dexamethasone. We also investigated the expression pattern of OB, PPARγand GLUT4 gene and tried to explore the regulating mechanism of SOCS-3 inducing insulin resistance.The main results were summarized as following:1. 100 nmol/L insulin treated adipocyte 2h can increased the expression of PARγ,GLUT4 and SOCS-3 mRNA. But it can be no significantly effect on the expression of OB gene. The increase of GLUT4 induced by insulin, maybe first increased PPARγ, then PPARγcaused increase of GLUT4 mRNA. The expression of SOCS-3 increased, but did not cause insulin resistance.2. 100 nmol/L insulin and 20 mmol/L glucose treated the primary culture adipocyte. It can induce OB gene expression. The effect on PPARγ,GLUT4 and SOCS-3 mRNA were similar with 100noml/L insulin treated. The high insulin and high glucose can induce OB mRNA expression, that is similar with type 2 diabetes, they are hyperinsulinemia, hyperglycemia and hyperleptinemia.3. The expression of PPARγand GLUT4 decreased, SOCS-3 and OB increased in porcine adipocyte which was treated by 300 nmol/L Dex. Maybe the mass increased of SOCS-3 induced insulin resistance. Although insulin induced expression of SOCS-3, SOCS-3 was not enough to cause insulin resistance. We also found the increase of OB gene expression. Maybe OB had partial effect on Dex increased SOCS-3 expression.4. After the primary porcine adipocyte was treated with 300nmol/L Dex for 24h, Dex was taken out for 24h. Then,the cell was treated with 100 nmol/L insulin and leptin, respectively. The arrested effect on SOCS-3 expression can not be alleviated by newly additive insulin or leptin. Maybe Dex increased SOCS-3. After took out Dex, maybe the mRNA expression of SOCS-3 gene was decreased, but the protein of SOCS-3 was also high. So when the adipocyte was treated by insulin and leptin, the SOCS-3 gene expression can not be induced. The effect of insulin and leptin was suppressed by SOCS-3. Maybe the continuance and mass expression of SOCS-3 induced insulin resistance and leptin resistance.