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目的探讨运动对高脂饮食诱导的胰岛素抵抗大鼠脂肪组织中糖原合成酶激酶3β(GSK- 3β)表达的影响。方法将30只SPF级雄性Wistar大鼠随机分为2组,其中正常对照组10只,给予常规饲料喂养,模型组20只,给予高脂饲料喂养。模型组大鼠经喂养4周后制成胰岛素抵抗模型,将其随机分为2个亚组(即胰岛素抵抗组和运动干预组),2个亚组继续给予高脂饲料喂养,同时运动干预组大鼠每周进行5 d游泳运动,持续6周。采用Western-blot方法检测各组大鼠附睾脂肪组织中GSK-3β的表达；定期检测大鼠体重(BW)、空腹血糖(FPG)、血浆胰岛素(FINS)、血甘油三酯(TG)及胆固醇(TC)水平,并计算胰岛素敏感指数(ISI)。结果各组大鼠经高脂饲料喂养4周后,与正常对照组比较,模型组大鼠BW、FPG、FINS、TC、TG均显著升高(P＜0．05或0．01),ISI则明显降低(P＜0．01),提示胰岛素抵抗模型诱导成功。经6周运动干预后,与胰岛素抵抗组比较,运动干预组大鼠脂肪组织GSK-3β表达显著下降(P＜0．05),与正常对照组比较,差异无统计学意义(P＞0．05)。结论运动可下调胰岛素抵抗大鼠脂肪组织GSK-3β的表达,促进葡萄糖的摄取及糖原合成,县有改善胰岛素抵抗功能。
Objective To investigate the effect of exercise on the expression of glycogen synthase kinase 3β (GSK-3β) in adipose tissue induced by high-fat diet in rats with insulin resistance. Methods Thirty SPF male Wistar rats were randomly divided into two groups, of which 10 were normal control group and fed with normal diet. The model group was fed with high fat diet. Rats in model group were made into insulin resistance model by feeding for 4 weeks. They were randomly divided into 2 subgroups (ie insulin resistance group and exercise intervention group), 2 subgroups were fed with high fat diet and exercise intervention group Rats swimming 5 days a week for 6 weeks. Western blot was used to detect the expression of GSK-3β in the epididymal adipose tissue of rats in each group. The body weight (BW), fasting blood glucose (FPG), insulin (FINS), triglyceride (TG) and cholesterol (TC) levels, and calculate the insulin sensitivity index (ISI). Results Compared with the normal control group, the BW, FPG, FINS, TC, TG in model group were significantly increased (P <0.05 or 0.01), the ISI Was significantly lower (P <0.01), suggesting that successful induction of insulin resistance model. Compared with insulin resistance group, the expression of GSK-3β in adipose tissue of rats in exercise intervention group decreased significantly after 6 weeks of exercise intervention (P <0.05), but there was no significant difference compared with that of normal control group (P> 0.05). 05). Conclusion Exercise can down-regulate the expression of GSK-3β in adipose tissue of rats with insulin resistance, promote glucose uptake and glycogen synthesis, and improve the insulin resistance in the county.