低含量会导致肝脏能量代谢障碍,通过鱼类中与胺相关的蛋白质1-介导的线粒体裂变
Jibin Lin1, Xueshan Li1, Kangle Lu1
1State Key Laboratory for Mariculture Breeding, Fisheries College of Jimei University, Xiamen, PR China; Xiamen Key Laboratory for Feed Quality Testing and Safety Evaluation, Fisheries College, Jimei University, Xiamen, PR China.
低饮食通过cAMP/PKA/Drp1通路影响线粒体裂变,破坏鱼类的能量代谢. 恢复这种途径可以改善ATP水平和线粒体功能.
科学领域:
- 水生动物营养水生动物营养
- 鱼类生理学 鱼类生理学
- 线粒体生物学 线粒体生物学
背景情况:
- 低 (LP) 饮食会破坏鱼类的肝脏能量代谢.
- 在LP诱导的肝能量代谢障碍背后的精确机制需要进一步研究.
研究的目的:
- 阐明线粒体在LP诱导的能量代谢障碍中的作用.
- 在低条件下研究鱼类肝脏能量代谢中的cAMP/PKA/Drp1信号通路.
主要方法:
- 斑点海和斑马鱼被食不同度的饮食.
- 在LP条件下,肝细胞用Drp1敲击或PKA激活剂 (8Br-cAMP) 进行治疗.
- 用生物化学测定,电子显微镜和免疫光检测来评估线粒体功能,形态学和糖脂代谢.
主要成果:
- 在斑点海中,LP饮食降低了肝脏ATP,cAMP和PKA/Drp1酸化.
- 在LP治疗的肝细胞中,drp1的淘汰和PKA的激活增加了ATP度,改善了线粒体形态.
- 在食斑马鱼的LP饮食中药理上抑制Drp1或PKA激活也提高了ATP水平.
结论:
- 在鱼类中,cAMP/PKA/Drp1信号通路与LP诱导的肝能量代谢障碍有关.
- 准线粒体裂变机制可能提供一种策略,以减轻低饮食对鱼类能量代谢的不良影响.
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