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热应激激活大鼠骨骼肌中的 Akt/mTOR 信号通路。

Heat stress activates the Akt/mTOR signalling pathway in rat skeletal muscle.

机构信息

Graduate School of Health and Sports Science, Juntendo University, Inzai, Chiba, Japan.

出版信息

Acta Physiol (Oxf). 2013 Feb;207(2):416-26. doi: 10.1111/apha.12040. Epub 2012 Dec 14.

DOI:10.1111/apha.12040
PMID:23167446
Abstract

AIM

It is well known that various stimuli, such as mechanical stress and nutrients, induce muscle hypertrophy thorough the Akt/mTOR signalling pathway, which is a key mediator of protein synthesis and hypertrophy in skeletal muscle. It was recently reported that heat stress also induces an increase in muscle weight and muscle protein content. In addition, heat stress enhances Akt/mTOR signalling after one bout of resistance exercise. However, it remains unclear whether increased temperature itself stimulates the Akt/mTOR signalling pathway.

METHODS

Forty-two male Wistar rats (279.5 ± 1.2 g) were divided into a control group (CON) or one of five thermal stress groups at 37, 38, 39, 40 or 41 °C (n = 7 each group). After overnight fasting, both legs were immersed in different temperatures of hot water for 30 min under sodium pentobarbital anaesthesia. The soleus and plantaris muscles were immediately removed from both legs after the thermal stress.

RESULTS

The phosphorylation of mTOR or 4E-BP1 and heat shock protein (HSP) expression levels were similar among groups in both the soleus and plantaris muscles. However, Akt and p70S6K phosphorylation significantly increased at 41 °C in the soleus and plantaris muscles. Moreover, we observed a temperature-dependent increase in Akt and p70S6K phosphorylation in both muscles.

CONCLUSION

Our data indicate that the altered temperature increased phosphorylation in a temperature-dependent manner in rat skeletal muscle and may itself be a key stimulator of Akt/mTOR signalling.

摘要

目的

众所周知,各种刺激因素,如机械应激和营养物质,通过 Akt/mTOR 信号通路诱导肌肉肥大,该通路是骨骼肌中蛋白质合成和肥大的关键介质。最近有报道称,热应激也会导致肌肉重量和肌肉蛋白含量增加。此外,热应激增强了一次抗阻运动后的 Akt/mTOR 信号。然而,目前尚不清楚温度升高本身是否会刺激 Akt/mTOR 信号通路。

方法

42 只雄性 Wistar 大鼠(279.5 ± 1.2 g)分为对照组(CON)或 37、38、39、40 或 41°C 五个热应激组中的一个(每组 7 只)。在隔夜禁食后,大鼠在戊巴比妥钠麻醉下将双腿浸入不同温度的热水中 30 分钟。热应激后,立即从双腿中取出比目鱼肌和跖肌。

结果

在比目鱼肌和跖肌中,mTOR 或 4E-BP1 的磷酸化和热休克蛋白(HSP)表达水平在各组之间相似。然而,在比目鱼肌和跖肌中,Akt 和 p70S6K 的磷酸化在 41°C 时显著增加。此外,我们观察到两种肌肉中 Akt 和 p70S6K 磷酸化呈温度依赖性增加。

结论

我们的数据表明,改变的温度以温度依赖的方式增加了大鼠骨骼肌中的磷酸化,并且本身可能是 Akt/mTOR 信号的关键刺激因素。

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