4周高强度间歇训练(HIIT)对2型糖尿病大鼠腓肠肌上下游mTORC1通路含量的影响

Golnaz Faezi, M. S. Moghadam, S. - Shadmehri, M. Fathalipour
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引用次数: 2

摘要

背景:mTORC1通路是蛋白质合成中最重要的通路之一,2型糖尿病和胰岛素抵抗可导致该通路的抑制。本研究旨在探讨4周高强度间歇训练(HIIT)对2型糖尿病大鼠腓肠肌上下游mTORC1通路含量的影响。材料与方法:本实验选取16只平均体重为250±20 gr的雄性Sprague-Dawley大鼠,经链脲佐菌素和烟酰胺诱导糖尿病后,随机分为糖尿病HIIT训练组和糖尿病对照组。实验组每周进行4天的运动训练,连续4周,对照组不进行任何训练计划。采用独立t检验对数据进行分析。结果:与对照组相比,HIIT训练组的AKT1蛋白总含量(p<0.31)、P70S6K1蛋白总含量(p<0.69)、4EBP1蛋白总含量(p<0.84)均无显著变化,而mTOR蛋白总含量(p<0.02)、AKT1蛋白磷酸化形式(p<0.03)、mTOR蛋白磷酸化形式(p<0.03)、P70S6K1蛋白磷酸化形式(p<0.009)均有显著升高。结论:HIIT训练可能激活mTORC1通路中的AKT1/mTOR/P70S6K1和AKT1/mTOR/4EBP1通路;因此,HIIT训练可以通过训练大鼠腓肠肌的这一途径导致蛋白质合成或肌肉肥大
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The effect of 4 weeks high-intensity interval training (HIIT) on the content of downstream and upstream mTORC1 pathways gastrocnemius muscle of type 2 diabetic rats
Background: The pathway of mTORC1 is one of the most important pathway in protein synthesis, and type 2 diabetes and insulin resistance can lead to inhibit this pathway. The aim of this study was to investigate the effect of 4 weeks high-intensity interval training (HIIT) on the content of downstream and upstream mTORC1 pathways in gastrocnemius muscle in type 2 diabetic rats. Materials and methods: In this experimental study, 16 Sprague-Dawley male rats (with mean weight of 250 ± 20 gr) were selected and after induction of diabetes by streptozotocin and nicotinamide, the rats were randomly assigned into two groups, including diabetic HIIT training and diabetic control. The experimental group performed 4 days a week the exercise training for 4 weeks, while the control group did not have any training program. Independent T-test was used to analyze the data. Results: A significant change was not observed in the total content of AKT1 proteins (p<0.31), P70S6K1 (p<0.69) and 4EBP1 (p<0.84) in the HIIT training group compared to the control group, but the total protein content of mTOR (p<0.02) and the form of phosphorylation of AKT1 (p<0.03), mTOR (p<0.03), P70S6K1 (p<0.02) and 4EBP1 (p<0.009) proteins showed significant increase in training group compared to the control group. Conclusion: The HIIT training can probably activate the pathway of AKT1/mTOR/P70S6K1 and AKT1/mTOR/4EBP1 in the mTORC1 pathway; therefore, the HIIT training can lead to protein synthesis or muscle hypertrophy through this pathway in the gastrocnemius muscle of the trained rats
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