亚迪波涅丁通过小鼠骨肌肉中的APPL1/p38MAPK/PGC-1α信号通路对虹膜蛋白的表达进行上调
Ruiqi Huang1, Sitong Xu2, Qi Guo3
1Department of College of Exercise and Health, Shenyang Sport University, Shenyang, Liaoning, China; Department of School of Physical Education, Liaoning Normal University, Dalian, Liaoning, China.
Molecular and cellular endocrinology
|February 7, 2026
概括
阿迪波涅丁通过APPL1/p38 MAPK/PGC-1α通路在骨肌肉中增强虹膜素的产生. 这种机制可以改善胰岛素敏感性,特别是在肥胖患者中.
科学领域:
- 内分泌学 在内分泌学.
- 代谢过程中的代谢.
- 分子生物学分子生物学
背景情况:
- 和虹膜素是能量恒温的关键调节剂.
- 已知它们与氧酶增殖器激活受体协活性剂1α (PGC-1α) 的相互作用,但信号连接尚不清楚.
研究的目的:
- 为了研究连接阿迪波内克丁和虹膜素的信号通路.
- 确定APPL1/p38 MAPK/PGC-1α通路在这种相互作用中的作用.
- 探索肥胖引起的胰岛素耐药性的影响.
主要方法:
- 在体内和体外研究中利用了阿迪波涅克丁淘汰赛 (KO) 小鼠和C2C12神经管细胞.
- 服用阿迪波内克丁,并使用机械拉伸.
- 分析了APPL1/p38 MAPK/PGC-1α信号通路中的关键蛋白质的表达.
主要成果:
- 皮菌素缺乏症降低了骨肌肉中的虹膜素和APPL1/p38 MAPK/PGC-1α信号传递.
- 服用阿迪波内克丁和炼可以逆转这些效应.
- 肥胖导致了这种途径的失调,抑制了虹膜素的合成和分泌.
- 肌管的机械拉伸模仿了这些体内发现.
结论:
- 在小鼠骨肌中,阿迪波涅通过APPL1/p38 MAPK/PGC-1α通路对虹膜蛋白进行上调.
- 这种途径的激活增强了胰岛素敏感性,为代谢障碍提供了潜在的治疗点.
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