摘要
目的:观察运动、膳食干预对胰岛素抵抗肥胖大鼠肝脏细胞因子信号抑制蛋白3(SOCS3)、胰岛素受体底物1(IRS-1)蛋白水平的影响,探讨运动、膳食干预对胰岛素抵抗大鼠信号通路的作用机制。方法:以高脂膳食诱导肥胖伴有胰岛素抵抗大鼠动物模型。将大鼠随机分为高脂膳食对照组(HH)、高脂膳食运动组(HHE)、普通膳食运动组(HNE)、普通膳食组(HN)及原有空白对照组(NN)。运动、膳食干预8周后,采用Western blot法检测各组大鼠肝脏中SOCS3、IRS-1水平;放射免疫法测定血清胰岛素(FINS)水平。结果:(1)各组大鼠肝脏IRS-1蛋白水平无明显差异。(2)HH组与NN组大鼠肝脏SOCS3蛋白水平无显著性差异,HNE组大鼠肝脏SOCS3蛋白较HH组及NN组显著下降(P<0.01),且显著低于HHE及HN组(P<0.01)。(3)大鼠胰岛素释放试验(IRT)中,在各时间点,HH组大鼠体内胰岛素浓度均显著高于其余各组(P<0.01);60 min及120 min时间点,HHE组大鼠血清胰岛素浓度显著高于NN组(P<0.05)。结论:运动联合膳食干预可以显著下调大鼠肝脏SOCS3蛋白水平。SOCS3水平的下调减少IRS-1蛋白降解可能并非是改善肥胖大鼠胰岛素抵抗的主要机制。
Objective To observe the changes in suppressor of cytokine signaling 3（SOCS3）and insulin receptor substrate-1（IRS-1）in liver,in order to study the mechanism and effect of exercise and diet interventions on the insulin resistance in obese rats. Methods Insulin resistance（IR）and dietary obesity were established in 40 male SD rats by feeding high-fat diet,and then the rats were randomized into four groups：high fat diet group（HH）,high fat diet combined with exercise group（HHE）,ordinary diet combined with exercise group（HNE）,ordinary diet group（HN）. Another 10 healthy male SD rats were served as blank control group（NN）。 The exercise and diet intervention lasted for 8 weeks. The SOCS3 and IRS-1 in liver were determined by Western blot and serum insulin by radioimmunity.Results After interventions,（1）there was no significant difference in liver IRS-1 among all groups;（2）no significant difference in liver SOCS3 was found between HH group and NN group,while SOCS3 was significantly lower only in HNE group than that in HH and NN groups（P 〈 0.01）,while SOCS3 was significantly lower only in HNE group than that in HH and NN groups（P 〈 0.01）;（3）insulin in HH group was higher than that in other groups at all time points of insulin releasing test（P 〈 0.01）,and in HHE group was higher than that in NN group at 60,120 minute of the test（P 〈 0.05）. Conclusions Exercise combined with diet can decrease liver SOCS3 level of obese rats with insulin resistance without significant effect on liver IRS-1,indicating that degradation of IRS-1 induced by SOCS3 down regulation may not be a key mechanism in improving insulin resistance of obese rats.
出处
《中国运动医学杂志》
CAS
CSCD
北大核心
2014年第8期797-803,共7页
Chinese Journal of Sports Medicine
基金
南京邮电大学人才引进科研启动基金(NY210086)
