| Obesity is excessive body fat tissue or abnormal fat distribution,and highly correlated with insulin resistance.Therefore,the function of adipose tissue in IR is becoming the focus of the recent survey.The hormones and cytokines which are secreted by adipose tissue are very important in the regulation of glycolysis and metabolize.Adipose tissue secretion of many biologically active substances in the body control sugar metabolism and energy metabolism balance plays an important role,TNF-αis one of many biologically active factors to the occurrence and development of insulin resistance plays an important role.The over-expression of TNF-αin adipose tissue can influence the insulin-sensitivity of fat,muscle and other tissue by autocrine and(or) paracrine to interfere the insulin receptor signal transduction,and impact the utilization of glucose.TNF-αaffect the insulin signal transduction through the serine sites on the insulin receptor,make insulin receptor substrate -1 serine phosphorylation,restrain IRS-1 tyrosine phosphorylation and phosphatidylinositol -3 kinase activity to damage the insulin signaling pathway,then inhibit the insulin signal transduction.Protein kinase B(PKB) is the key factor of phosphatidylinositol -3 kinase (PI-3K) pathway and it's the necessary material in insulin-stimulated glucose transporter. TNF-αregulate the production of FFA and make IRS-1 serine phosphorylation in order to restrain its tyrosine phosphorylation,to regulate the expression of PKB in adipose tissue, induce IR in adipose tissue.Purpose:Large number of studies confirms that exercise can reform insulin resistance,and the influence of exercise on TNF-αin serum and adipose tissue in the different forms of exercise are not the same.In recent years the study of insulin resistance has shifted to its pathway.Exercise can increase PKB in adipose tissue,it is necessary to explore the possibility of exercise by changing the blood and adipose tissue TNF-αlevels to improve insulin resistance.In the PI-3K pathway,whether PKB to play a role? This study was 8 weeks treadmill training in rats with high fat diet on insulin resistance in the formation of intervention,researching Treadmill Training how to affect TNF-αin rats fed with high fat diet on insulin resistance in the process of formation of the insulin receptor signal PI-3K transduction pathway,that adipose tissue TNF-αin the exercise to improve insulin resistance in the process of role to explore the treadmill training in rats fed with high fat diet on adipose tissue insulin receptor signal transduction pathway after the effects of TNF-αmechanism.Methods:30 male SD rats were randomly divided into control group(C),high-fat group(H), high-fat exercise group(HE) and exercise group(E),the control group and exercise group was ordinary feeding,high-fat group and high-fat exercise group was fed high fat diet.High fat diet and normal diet calorie rat were 35%and 11%.High-fat group and exercise group had an 8-week treadmill exercise for the same time.5 days a week,one hour per day,running a gradient of 0°angle,speed for 20m/min.ELISA was used to evaluate the TNF-αin adipose tissue,and Western blot analysis was used to test the expression level of PKB in adipose tissue.Results:①After experiment weights and the average weight gain of high-fat group rats are highest,compared with other three groups difference was significant(P＜0.05 or P＜0.01).②Convert the food intake into the corresponding heat,the calorie intake of high-fat group rats are highest in the 8 experimental weeks,and compared with the control group and exercise group rats the difference was significant(P＜0.01).③Various indicators of body fat of high-fat group rats are highest,compared with other three groups difference was significant(P＜0.05 or P＜0.01).④Blood sugar levels in 4 group rats have no significant differences; serum insulin levels of high-fat group rats are highest,the insulin sensitivity index of high-fat group rats was lower than the control group and exercise group rats,the difference was significant(P＜0.05 or P＜0.01).The serum TNF-αof high-fat exercise group rats are highest, compared with other three groups difference was significant(P＜0.05 or P＜0.01).⑤after 8 week-experiment,the adipose tissue TNF-αof high-fat group rats are highest,compared with other three groups difference was significant(P＜0.05 or P＜0.01);the adipose tissue TNF-αof exercise group rats are lowest,compared with high-fat exercise group rats difference was significant(P＜0.01).The adipose tissue PKB of high-fat group rats are lowest,compared with other three groups difference was significant(P＜0.05 or P＜0.01);the adipose tissue TNF-αof exercise group rats are higher than control group rats,difference was significant(P ＜0.01).⑥Correlation analysis found that the expression of adipose tissue TNF-αin the rats moderately correlated with serum insulin levels and low correlated with body weight,body fat ratio,epididymal and perirenal fat total weight,and weakly correlated with serum TNF-α. Adipose tissue TNF-αis negatively moderately correlated with adipose tissue PKB and insulin sensitivity index.The expression of adipose tissue PKB in the rats negatively moderately correlated with body weight,body fat ratio,epididymal,perirenal fat total weight and serum insulin levels,and low correlated with insulin sensitivity index,and weakly correlated with serum TNF-α.Conclusions:1.Through the eight-week high-fat diet fed the adipose tissue TNF-αof rats are increased and the adipose tissue PKB are decreased,and promoted the occurrence and development of insulin resistance;and treadmill training at the same time confronts this phenomenon,decrease the adipose tissue TNF-α,increase the adipose tissue PKB that will good to slow or prevent the development of insulin resistance with high-fat diet.2.The adipose tissue secreted TNF-αmay regulate the adipose tissue PKB.Treadmill training may reduce adipose tissue TNF-αof high-fat-diet rats to regulate of adipose tissue PKB,and then affect PI-3K transduction that will good to slow or prevent the development of insulin resistance with high-fat diet.
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