Abstract：
Exercise-induced physical endurance enhancement and skeletal muscle remodeling can prevent and delay the development of multiple diseases, especially metabolic syndrome. Herein, the study explored the association between glucagon-like peptide-1 (GLP-1) secretion and exercise, and its effect on skeletal muscle remodeling to enhance endurance capacity. We found both acute exercise and short-term endurance training significantly increased the secretion of GLP-1 in mice. Recombinant adeno-associated virus (AAV) encoding Gcg (proglucagon) was used to induce the overexpression of GLP-1 in skeletal muscle of mice. Overexpression of GLP-1 in skeletal muscle enhanced endurance capacity. Meanwhile, glycogen synthesis, glucose uptake, type I fibers proportion, and mitochondrial biogenesis were augmented in GLP-1-AAV skeletal muscle. Furthermore, the in vitro experiment showed that exendin-4 (a GLP-1 receptor agonist) treatment remarkably promoted glucose uptake, type I fibers formation, and mitochondrial respiration. Mechanistically, the knockdown of AMPK could reverse the effects imposed by GLP-1R activation in vitro. Taken together, these results verify that GLP-1 regulates skeletal muscle remodeling to enhance exercise endurance possibly via GLP-1R signaling-mediated phosphorylation of AMPK.
摘要：
运动引起的身体耐力增强和骨骼肌重塑可以预防和延缓多种疾病的发展，尤其是代谢综合征.在这里，这项研究探讨了胰高血糖素样肽-1（GLP-1）分泌与运动之间的关系，及其对骨骼肌重塑的影响，以增强耐力。我们发现急性运动和短期耐力训练均显着增加小鼠GLP-1的分泌。使用编码Gcg(胰高血糖素原)的重组腺相关病毒(AAV)诱导GLP-1在小鼠骨骼肌中的过表达。GLP-1在骨骼肌中的过表达增强了耐力。同时,糖原合成，葡萄糖摄取，I型纤维比例，线粒体生物发生在GLP-1-AAV骨骼肌中增强。此外，体外实验表明，exendin-4（GLP-1受体激动剂）治疗显著促进葡萄糖摄取，I型纤维的形成，和线粒体呼吸。机械上,AMPK的敲减可以在体外逆转GLP-1R激活的作用。一起来看,这些结果证实GLP-1可能通过GLP-1R信号介导的AMPK磷酸化调节骨骼肌重塑以增强运动耐力.
