代谢相关脂肪性肝病(MAFLD)是人类和哺乳动物肝脏脂肪沉积引起的慢性肝病,而脂肪肝出血性综合征(FLHS)是蛋鸡的一种脂肪肝病,可增加其死亡率,给蛋鸡产业造成严重的经济损失。越来越多的证据表明脂肪肝疾病的发生与线粒体稳态的破坏之间存在密切关系。研究证明牛磺酸能调节肝脏脂肪代谢,减少肝脏脂肪沉积,抑制氧化应激,减轻线粒体功能障碍.然而,牛磺酸调节肝细胞线粒体稳态的机制需要进一步研究。在这项研究中,我们确定了牛磺酸对高能低蛋白饮食诱导的产蛋鸡FLHS和游离脂肪酸(FFA)诱导的脂肪变性培养肝细胞的影响和机制。肝功能,脂质代谢,抗氧化能力,线粒体功能,线粒体动力学,自噬,并检测到生物合成。结果显示肝脏结构和功能受损,线粒体损伤和功能障碍,脂质积累,线粒体融合和裂变之间的不平衡,线粒体自噬,和FLHS母鸡和脂肪变性肝细胞的生物合成。牛磺酸给药可显著抑制FLHS的发生,保护肝细胞中的线粒体免受脂质积累和FFA诱导的疾病,上调Mfn1,Mfn2,Opa1,LC3I的表达水平,LC3II,PINK1,PGC-1α,Nrf1、Nrf2和Tfam,并下调Fis1、Drp1和p62的表达水平。总之,牛磺酸可以通过调节线粒体稳态来保护蛋鸡免受FLHS的侵害,包括线粒体动力学的调节,自噬,和生物合成。
Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease caused by fat deposition in the liver of humans and mammals, while fatty liver hemorrhagic syndrome (FLHS) is a fatty liver disease in laying hens which can increase the mortality and cause severe economic losses to the laying industry. Increasing evidence has shown a close relationship between the occurrence of fatty liver disease and the disruption of mitochondrial homeostasis. Studies have proven that taurine can regulate hepatic fat metabolism, reduce hepatic fatty deposition, inhibit oxidative stress, and alleviate mitochondrial dysfunction. However, the mechanisms by which taurine regulates mitochondrial homeostasis in hepatocytes need to be further studied. In this study, we determined the effects and mechanisms of taurine on high-energy low-protein diet-induced FLHS in laying hens and in cultured hepatocytes in free fatty acid (FFA)-induced steatosis. The liver function, lipid metabolism, antioxidant capacity, mitochondrial function, mitochondrial dynamics, autophagy, and biosynthesis were detected. The results showed impaired liver structure and function, mitochondrial damage and dysfunction, lipid accumulation, and imbalance between mitochondrial fusion and fission, mitochondrial autophagy, and biosynthesis in both FLHS hens and steatosis hepatocytes. Taurine administration can significantly inhibit the occurrence of FLHS, protect mitochondria in hepatocytes from disease induced by lipid accumulation and FFA, up-regulate the expression levels of Mfn1, Mfn2, Opa1, LC3I, LC3II, PINK1, PGC-1α, Nrf1, Nrf2, and Tfam, and down-regulate the expression levels of Fis1, Drp1, and p62. In conclusion, taurine can protect laying hens from FLHS through the regulation of mitochondrial homeostasis, including the regulation of mitochondrial dynamics, autophagy, and biosynthesis.