帕帕α激活通过脂质代谢独立路径刺激自流
Yan-Yu Zhang1, Jun-Xian Wang1, Fang Qiao1
1LANEH, School of Life Sciences, East China Normal University, Shanghai, China.
Fish physiology and biochemistry
|February 24, 2024
概括
过氧体增殖器激活受体α (PPARα) 激活通过调节转录因子EB (TFEB) 来增强自,独立于脂质代谢. 这一发现为管理水产养殖中的肝脂积累提供了洞察力.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 水产养殖营养水产养殖营养
背景情况:
- 自会通过自和溶酶体降解细胞组分.
- 线粒体脂肪酸氧化 (FAO) 和自是相互关联的,抑制的FAO诱导自.
- 过氧体增殖器激活受体α (PPARα) 影响脂质代谢和自,可能通过转录因子EB (TFEB).
研究的目的:
- 调查PPARα是否通过TFEB转录控制或线粒体FAO来调节自.
- 通过检查脂质催化和自之间的联系,探索水产养殖中的降脂策略.
- 评估纤维酸 (PPARα激活剂) 和L-卡尼丁 (粮农组织增强剂) 对尼罗河鱼的自的作用.
主要方法:
- 对尼罗河鱼的食中注射费诺纤维酸和L-卡尼丁.
- 测量肝脂含量和ATP的产生.
- 对自蛋白水平 (LC3II,p62),自流量,TFEB表达和核转位的分析.
- 在PPARα激活研究中包括斑马鱼肝细胞.
主要成果:
- 费诺纤维酸和L-卡尼丁降低了肝脂含量,增加了ATP的产生;费诺纤维酸更有效.
- L-卡尼丁增强了FAO,但没有改变自蛋白水平或流量.
- 纤维酸激活的PPARα促进了TFEB表达和核转位,升调了自开始和溶酶体生物发生基因.
- PPARα激活显示了LC3II和p62蛋白质增加的趋势,这表明自流的增强独立于脂质代谢.
结论:
- PPARα激活诱导自流,主要通过TFEB转录调节.
- 由PPARα激活引起的自流是独立于线粒体FAO的变化.
- 这些发现为开发营养策略提供了基础,以控制鱼类肝脏脂质积累.
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