跑台运动对Fetuin-A诱导的胰岛素抵抗鼠MAPK和Akt磷酸化的影响

Effects of Exercise on MAPK,Akt Phosphorylation of Fetuin-A-induced Insulin Resistance Mice

目的:研究跑台运动对Fetuin-A诱导的胰岛素抵抗鼠肝脏MAPK和骨骼肌Akt磷酸化的影响,探索运动缓解Fetuin-A诱导的胰岛素抵抗的肝脏和骨骼肌机制。方法:牛fetuin-A注射建立胰岛素抵抗鼠模型。设一次性运动组(FOE)、8周运动组(FAE)、安静对照组(FC)和正常安静对照组(C)。免疫印记法、RT-PCR法检测骨骼肌、肝脏和血液的相关指标。结果:(1)与C组相比,各组实验鼠血清Fetuin-A、HOMA-IR和肝脏PEPCK表达均显著增加(P<0.01),肝脏MAPK磷酸化、GK表达和肝糖原均显著减少(P<0.01);骨骼肌Akt磷酸化、GLUT4表达和葡萄糖摄取率均显著减少(P<0.01)。(2)与FC组相比,FAE组肝脏MAPK磷酸化、GK表达和肝糖原含量均显著增加(P<0.01),PEPCK表达显著降低(P<0.01);FOE组和FAE组骨骼肌Akt磷酸化、GLUT4表达和葡萄糖摄取率均显著增加(P<0.01)。结论:运动能够显著改善Fetuin-A诱导的胰岛素抵抗,机制涉及运动后肝脏MAPK磷酸化和骨骼肌Akt磷酸化增加,从而减少肝脏向血液过量释放葡萄糖,并增加骨骼肌葡萄糖摄取。

Objectivity：To study effects of exercise on MAPK and Akt phosphorylation of Fe- tuin -A - induced insul in resistance mice, and explored the mechanism of exercise intervention in Fetuin - A - induced insulin resistance. Method ： Fetuin - A - induced insulin resistance mice established by Fetuin -A intraperitoneal injection. Model rats divided in Fe- tuin - A one time exercise group （ FOE ）, Fetuin - A aerobic exercise group （ FAE ）, Fetuin - A control group （ FC ）, and control group （ C ）. Results ： （ 1 ） Fetuin - A, HOMA - IR, and liver PEPCK expression increased more in group FC, group FAE and group FAE than groupC, respectively. Liver MAPK phosphorylation, GKexpression, and hepatic glycogen decreased more in group FC, group FAE and group FAE than group C, respectively. Skeletal muscle Akt phosphorylation, GLUT4 expression, and glucose uptake ratio decreased more in group FC,group FAE and group FAE than group C, respectively. （2） Liver MAPK phosphorylation, GK expression, and hepatic glycogen increased more in group FAE than groupFC,respective- ly. Skeletal muscle Akt phosphorylation, GLUT4 expression, and glucose uptake ratio in- creased more in group FOE and group FAE than group FC, respectively. Conclusions：Aerobic exercise could decrease HOMA - IR in Fetuin - A - induced insulin resistance mice, improve insulin resistance through increasing liver MAPK phosphorylation, and skeletal muscle Akt phosphorylation. This mechanism involve decreasing hepatic glycose releasing and increasing uptake ratio in skeletal muscle.