AMPK和PPARdelta激动剂是运动模仿剂
Vihang A Narkar1, Michael Downes, Ruth T Yu
1Gene Expression Laboratory, Salk Institute, La Jolla, CA 92037, USA.
Cell
|August 5, 2008
概括
研究人员发现,用药物准AMPK-PPARdelta通路可以提高跑步耐力. 一种口服活性药物AICAR显著增加了小鼠的耐力,即使没有运动,也为代谢疾病治疗提供了潜力.
科学领域:
- 运动生理学 运动生理学
- 代谢性疾病研究研究.
- 药理干预措施 药理干预措施
背景情况:
- 耐力运动对健康有好处,激励人们寻找可模仿或增强其对代谢疾病影响的药物.
- 像白醇这样的天然化合物表现出增强耐力的特性,但它们的代谢点尚不清楚.
- 确定运动激活的特定分子通路对于开发向疗法至关重要.
研究的目的:
- 研究路径特异性药物对小鼠耐力能力的影响.
- 为了确定是否针对AMPK-PPARdelta途径可以增强运动适应性或提高耐力,独立于运动.
主要方法:
- 用跑步机跑步测试来评估小鼠的耐力.
- 评估了PPARbeta/delta激动剂和AICAR (AMPK激动剂) 对跑步耐力和肌肉特征的影响.
- 与代谢途径相关的基因表达被分析为对AICAR治疗的反应.
主要成果:
- 运动训练和PPARbeta/delta激动剂协同增加了小鼠的氧化肌肉纤维和跑步耐力.
- 在静坐性小鼠中,单独使用AICAR治疗在4周后显著提高了44%的跑步耐力.
- 艾卡尔治疗诱导了关键的代谢基因,这表明观察到的耐力增强的分子基础.
结论:
- AMPK-PPARdelta通路是药理干预改善耐力的一个可行的目标.
- 针对这种途径的口服活性药物可以增强训练适应性.
- 药理上激活AMPK-PPARdelta通路,即使在没有运动的情况下也可以增加耐力,为代谢疾病提供一种新的治疗策略.
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