Fasting enhances cold resistance in fish through stimulating lipid catabolism and autophagy
Fasting enhances cold resistance in fish through stimulating lipid catabolism and autophagy
复制标题
禁食通过刺激脂质分解代谢和自噬增强鱼类的抗寒能力
DOI：
10.1113/jp277091
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发表时间：
2019-03-15
影响因子：
5.5
通讯作者：
Du, Zhen-Yu
中科院分区：
文献类型：
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作者：
Lu, Dong-Liang;Ma, Qiang;Du, Zhen-Yu
在寒冷的环境中，哺乳动物会增加食物摄入量，而鱼类则会减少或停止进食。然而，鱼类在抗寒过程中禁食的生理价值目前尚不清楚。禁食48 h以上可增强斑马鱼的急性抗寒能力，这与脂质代谢和细胞损伤减弱有关。脂质过氧化和自噬是鱼类抗寒所必需的，抑制线粒体脂肪酸β-氧化或自噬可减弱禁食诱导的抗寒性。雷帕霉素对雷帕霉素机制靶点（mTOR）信号通路的抑制在很大程度上模拟了禁食在促进抗寒性方面的有益作用，表明mTOR信号通路可能参与了禁食诱导的鱼类抗寒性。我们的研究表明，禁食可能是鱼类在冷应激下生存的一种保护策略。
In a cold environment, mammals increase their food intake while fish decrease or stop feeding. However, the physiological value of fasting during cold resistance in fish is currently unknown. Fasting for more than 48 h enhanced acute cold resistance in zebrafish, which correlated with lipid catabolism and cell damage attenuation. Lipid catabolism and autophagy were necessary for cold resistance in fish and the inhibition of mitochondrial fatty acid β‐oxidation or autophagy weakened the fasting‐induced cold resistance. Repression of mechanistic target of rapamycin (mTOR) signalling pathway by rapamycin largely mimicked the beneficial effects of fasting in promoting cold resistance, suggesting mTOR signalling may be involved in the fasting‐induced cold resistance in fish. Our study demonstrates that fasting may be a protective strategy for fish to survive under cold stress.