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首页> 外文期刊>Experimental Physiology >Muscle glycogen resynthesis, signalling and metabolic responses following acute exercise in exercise-trained pigs carrying the PRKAG3 mutation.
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Muscle glycogen resynthesis, signalling and metabolic responses following acute exercise in exercise-trained pigs carrying the PRKAG3 mutation.

机译：接受PRKAG3突变的运动训练猪进行急性运动后，肌肉糖原的再合成，信号传导和代谢反应。

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Hampshire pigs carrying the PRKAG3 mutation in the AMP-activated protein kinase (AMPK) gamma3 subunit exhibit excessive skeletal muscle glycogen storage and an altered glycogen synthesis signalling response following exercise. AMPK plays an important role as a regulator of carbohydrate and fat metabolism in mammalian cells. Exercise-trained muscles are repeatedly exposed to glycogen degradation and resynthesis, to which the signalling pathways adapt. The aim of this study was to examine the effect of acute exercise on glycogen synthesis signalling pathways, and the levels of insulin and other substrates in blood in exercise-trained pigs with and without the PRKAG3 mutation. After 5 weeks of training, pigs performed two standardized treadmill exercise tests, and skeletal muscle biopsies were obtained immediately after exercise and 3 h postexercise in the first test, and 6 h postexercise in the second test. The PRKAG3 mutation carriers had higher glycogen storage, and resynthesis of glycogen was faster after 3 h but not after 6 h of recovery. Alterations in the concentrations of insulin, glucose, lactate and free fatty acids after exercise did not differ between the genotypes. The carriers showed a lower expression of AMPK and increased phosphorylation of Akt Ser(473) after exercise, compared with non-carriers. Acute exercise stimulated the phosphorylation of AS160 in both genotypes, and the phosphorylation of GSK3alpha Ser(21) and ACC Ser(79) in the non-carriers. In conclusion, exercise-trained pigs carrying the PRKAG3 mutation show an altered Akt and AMPK signalling response to acute exercise, indicating that glucose metabolism is associated with faster resynthesis of muscle glycogen in this group.
机译：汉普郡猪在AMP激活的蛋白激酶（AMPK）gamma3亚基中携带PRKAG3突变，其骨骼肌糖原存储过多，运动后糖原合成信号反应发生变化。 AMPK作为哺乳动物细胞中碳水化合物和脂肪代谢的调节剂发挥着重要作用。训练有素的肌肉反复暴露于糖原降解和再合成，信号通路适应于此。这项研究的目的是检验急性运动对糖原合成信号传导途径的影响，以及在运动训练的猪中是否存在PRKAG3突变的血液中胰岛素和其他底物的水平。经过5周的训练，猪进行了两次标准化的跑步机运动测试，运动后立即进行骨骼肌活检，第一次测试进行3h，第二次测试进行6h。 PRKAG3突变携带者具有更高的糖原储存能力，并且糖原的再合成在3小时后恢复更快，但在恢复6小时后却没有。运动后胰岛素，葡萄糖，乳酸和游离脂肪酸的浓度变化在基因型之间没有差异。与非载体相比，载体在运动后显示出较低的AMPK表达并增加Akt Ser（473）的磷酸化。急性运动会刺激两种基因型的AS160的磷酸化，以及在非携带者中刺激GSK3alpha Ser（21）和ACC Ser（79）的磷酸化。总之，经过运动训练的带有PRKAG3突变的猪对急性运动表现出改变的Akt和AMPK信号反应，表明该组中的葡萄糖代谢与肌肉糖原的更快再合成有关。

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