Taurine attenuates the development of hepatic steatosis through the inhibition of oxidative stress in a model of nonalcoholic fatty liver disease in vivo and in vitro
Amino Acids, ISSN: 1438-2199, Vol: 50, Issue: 9, Page: 1279-1288
2018
- 59Citations
- 46Captures
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Metrics Details
- Citations59
- Citation Indexes59
- 59
- Captures46
- Readers46
- 46
Article Description
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.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85049074462&origin=inward; http://dx.doi.org/10.1007/s00726-018-2605-8; http://www.ncbi.nlm.nih.gov/pubmed/29946793; http://link.springer.com/10.1007/s00726-018-2605-8; https://dx.doi.org/10.1007/s00726-018-2605-8; https://link.springer.com/article/10.1007/s00726-018-2605-8
Springer Science and Business Media LLC
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