Department of Bioscience and Biotechnology, Fukui Prefectural University, Eiheiji-cho, Fukui, 910-1195, Japan.
Clinical Trial Coordinating Center, Kitasato University, Minato-ku, Tokyo, 108-8643, Japan.
Amino Acids. 2018 Sep;50(9):1279-1288. doi: 10.1007/s00726-018-2605-8. Epub 2018 Jun 26.
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. It is characterized by the accumulation of triglyceride within hepatocytes. Taurine is a sulfur-containing-β-amino acid that is widely distributed in mammalian tissues. The objective of this study was to examine the effects of taurine on the development of hepatic steatosis in a model of NAFLD in vivo and in vitro. Male C57BL/6J mice were fed a high-fat diet (HFD) supplemented with 2% (w/v) or 5% (w/v) taurine for 12 weeks. An in vitro study was performed in HepG2 cells loaded with fatty acids. Twelve weeks of supplementation with an HFD increased the hepatic lipid levels and oxidative stress as well as the body weight and liver weight. Taurine significantly suppressed these changes, which was accompanied by a decrease in the hepatic level of thiobarbituric acid-reactive substances (TBARS). In addition, taurine treatment suppressed the HFD-induced reduction of the enzyme activity of hepatic superoxide dismutase and catalase and the reduction of the hepatic level of reduced glutathione and ATP. In HepG2 cells, taurine suppressed the fatty acid-induced lipid accumulation, production of reactive oxygen species and TBARS level, and amelioration of the fatty acid-induced disruption of the mitochondrial membrane potential. These results showed that taurine was effective in alleviating hepatic steatosis by reducing oxidative stress. Taurine may, therefore, be of therapeutic value in reducing the risks associated with NAFLD.
非酒精性脂肪性肝病(NAFLD)是最常见的慢性肝病病因。其特征为肝细胞内甘油三酯蓄积。牛磺酸是一种含硫的β-氨基酸,广泛分布于哺乳动物组织中。本研究旨在探讨牛磺酸对体内和体外 NAFLD 模型肝脂肪变性发展的影响。雄性 C57BL/6J 小鼠给予高脂肪饮食(HFD)并补充 2%(w/v)或 5%(w/v)牛磺酸,喂养 12 周。在负载脂肪酸的 HepG2 细胞中进行体外研究。12 周的 HFD 补充增加了肝内脂质水平和氧化应激以及体重和肝重。牛磺酸显著抑制了这些变化,同时肝内硫代巴比妥酸反应物质(TBARS)水平降低。此外,牛磺酸治疗抑制了 HFD 诱导的肝超氧化物歧化酶和过氧化氢酶活性降低以及肝还原型谷胱甘肽和 ATP 水平降低。在 HepG2 细胞中,牛磺酸抑制了脂肪酸诱导的脂质蓄积、活性氧的产生和 TBARS 水平的升高,并改善了脂肪酸诱导的线粒体膜电位破坏。这些结果表明,牛磺酸通过降低氧化应激有效缓解肝脂肪变性。因此,牛磺酸可能具有降低与 NAFLD 相关风险的治疗价值。