High Fat Diet Induced Insulin Resistance And The Influence To Interleukin 6, Tumor Necrosis Factor A And P-IKBα

Objective:Research on a high-fat diet C57 mice fed lead to insulin resistance,We compared the change of weight, fasting blood glucose and insulin level in surum between high-fat group and normal control group. Analysis the different expression of Interleukin-6 and nuclear Tumor necrosis factor-a in liver and Pancreas of insulin resistance (IR) mouse. Explore the role of adipose cell factors in the Pathogenesis of insulin resistance. To study the expressions of P-Ikb a in insulin resistance (IR)mouse Method:150 C57 mice were randomly assigned into 3 groups, the model group, insulin group, the insulin stimulate group and the normal control group. The first two groups were given high sugar and fat diet fed, the normal control group were given ordinary diet, all free water, a total of feeding 12 weeks. Monitor fasting blood glucose, weight change, establish insulin resistance model. Application the expression of IL-6 and TNF-a in liver, and Pancreas by immunohistochemistry. And the insulin level in serum were determined by radioimmunoassay. And the expression of P-Ikb a in liver, and pancreas were examined by Western blot.Result:High-fat feeding induced insulin resistance model success:IR was verified in model group, but not in NC group. The levels of the weight and the blood glucose in model group were markedly increased compared with NC group(p<0.05) Immunohistochemical results show that, The expression of IL-6 and TNF-a in tissues were markedly increased compared with NC group (P<0.05). The expression of P-Ikb a in tissues were markedly decreased compared with NC group (P <0.05). Conclusion:compared with NC group, the expression of IL-6 and TNF-a in IR model group mice were significantly increased, and The expression in liver was earlier than in Pancreas. Adipocytokines disorder were related with IR. The different role of adipocytokines attributed to the different onset of IR, which was one of Pathogenesis of insulin resistance. The expression of P-Ikb a in IR mice were significantly different in liver and pancreas.