Abstract
Several transporters have been identified for taurine (TAU) absorption from the gastrointestinal (GI) tract. The Na+/Cl--dependent taurine transporter (TauT) and PAT1 (SLC36A1) are well-known TAU transporters in the GI. These transporters efficiently deliver TAU from GI to the bloodstream. On the other hand, no metabolic pathway has been identified for TAU in the human body. But, it has been found that GI-resident bacteria are able to metabolize TAU to sulfur-containing chemicals (e.g., H2S). Hence, GI is the primary place for TAU metabolism. TAU-conjugated compounds such as bile acids are also excreted through GI. Compounds such as H2S could be re-absorbed from GI and have a tremendous physiological effect on other organs (e.g., heart and vessels). Finally, it should be noted that several studies mentioned that TAU could protect GI in various pathological conditions (e.g., xenobiotics-induced GI damage). In the current chapter, a brief review of the absorption, metabolism, and excretion of TAU is provided. Then, the importance of TAU metabolites in the GI and other organs is highlighted. Finally, the effects of TAU on GI complications are discussed, focusing on the effects of this amino acid on oxidative stress biomarkers and mitochondrial impairment. These data could give a new concept of the physiological roles of TAU as well as its effects on GI complications.