Taurine and the Liver: A Focus on Mitochondria-related Liver Disease

 Although the liver is the leading site for taurine (TAU) synthesis, the level of this amino acid in hepatic tissue is relatively low. It is well-known that TAU is efficiently redistributed from hepatocytes to the circulation. However, the human body’s capacity for TAU synthesis is negligible, and we receive a very high percentage of our body TAU from exogenous sources. Plasma TAU is taken up by several tissues, such as the skeletal muscle and the heart. The roles of TAU in liver function are the subject of many investigations. It has been found that TAU could have beneficial effects against xenobiotics-induced liver injury, alcoholism-associated hepatic damage, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), or even viral hepatitis infections. The inhibition of cytochrome P450, alleviation of oxidative stress, inhibition of inflammatory reactions, and the mitigation of tissue fibrosis are fundamental mechanisms proposed for the hepatoprotective properties of TAU. On the other hand, many studies indicate that hepatocytes’ mitochondria are essential targets for the cytoprotective properties of TAU. The current chapter reviews the beneficial role of TAU on the most common liver disorders, focusing on the effects of this amino acid on mitochondrial function and energy metabolism.