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首页> 美国卫生研究院文献>The Journal of Physiology >Exercise training and return to a well-balanced diet activate the neuregulin 1/ErbB pathway in skeletal muscle of obese rats
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Exercise training and return to a well-balanced diet activate the neuregulin 1/ErbB pathway in skeletal muscle of obese rats

机译：运动训练并恢复均衡饮食会激活肥胖大鼠骨骼肌中的神经调节蛋白1 / ErbB途径

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Some studies suggest that the signalling pathway of neuregulin 1 (NRG1), a protein involved in the regulation of skeletal muscle metabolism, could be altered by nutritional and exercise interventions. We hypothesized that diet-induced obesity could lead to alterations of the NRG1 signalling pathway and that chronic exercise could improve NRG1 signalling in rat skeletal muscle. To test this hypothesis, male Wistar rats received a high fat/high sucrose (HF/HS) diet for 16 weeks. At the end of this period, NRG1 and ErbB expression/activity in skeletal muscle was assessed. The obese rats then continued the HF/HS diet or were switched to a well-balanced diet. Moreover, in both groups, half of the animals also performed low intensity treadmill exercise training. After another 8 weeks, NRG1 and ErbB expression/activity in skeletal muscle were tested again. The 16 week HF/HS diet induced obesity, but did not significantly affect the NRG1/ErbB signalling pathway in rat skeletal muscle. Conversely, after the switch to a well-balanced diet, NRG1 cleavage ratio and ErbB4 amount were increased. Chronic exercise training also promoted NRG1 cleavage, resulting in increased ErbB4 phosphorylation. This result was associated with increased protein expression and phosphorylation ratio of the metalloprotease ADAM17, which is involved in NRG1 shedding. Similarly, in vitro stretch-induced activation of ADAM17 in rat myoblasts induced NRG1 cleavage and ErbB4 activation. These results show that low intensity endurance training and well-balanced diet activate the NRG1-ErbB4 pathway, possibly via the metalloprotease ADAM17, in skeletal muscle of diet-induced obese rats.
机译：一些研究表明，神经调节蛋白1（NRG1）的信号传导途径可能参与营养和运动干预，而神经调节蛋白1是参与骨骼肌代谢调节的蛋白质。我们假设饮食引起的肥胖症可能导致NRG1信号通路的改变，而长期运动可以改善大鼠骨骼肌中NRG1的信号。为了验证这一假设，雄性Wistar大鼠接受了高脂肪/高蔗糖（HF / HS）饮食16周。在此期间结束时，评估了骨骼肌中NRG1和ErbB的表达/活性。然后，肥胖大鼠继续进行HF / HS饮食，或改用均衡饮食。此外，在两组中，一半的动物还进行了低强度跑步机运动训练。再过8周后，再次测试骨骼肌中NRG1和ErbB的表达/活性。 16周HF / HS饮食诱导肥胖，但并未显着影响大鼠骨骼肌的NRG1 / ErbB信号通路。相反，改用均衡饮食后，NRG1裂解率和ErbB4量增加。长期运动训练还促进了NRG1的裂解，导致ErbB4磷酸化增加。该结果与增加的蛋白表达和金属蛋白酶ADAM17的磷酸化率有关，这与NRG1脱落有关。同样，大鼠成肌细胞中ADAM17的体外拉伸诱导激活可诱导NRG1裂解和ErbB4激活。这些结果表明，低强度耐力训练和均衡饮食可通过饮食诱导的肥胖大鼠骨骼肌中的金属蛋白酶ADAM17激活NRG1-ErbB4途径。

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