|Bauchart-Thevret, Caroline -|
|Stoll, Barbara -|
Submitted to: Nutrition Research Reviews
Publication Type: Review Article
Publication Acceptance Date: August 1, 2009
Publication Date: December 20, 2009
Citation: Bauchart-Thevret, C., Stoll, B., Burrin, D.G. 2009. Intestinal metabolism of sulfur amino acids. Nutrition Research Reviews. 22:175-187. Technical Abstract: The gastrointestinal tract (GIT) is a metabolically significant site of sulfur amino acid (SAA) metabolism in the body and metabolizes approx. 20% of the dietary methionine intake that is mainly transmethylated to homocysteine and transsulfurated to cysteine. The GIT accounts for approx. 25% of the whole-body transmethylation and transsulfuration. In addition, in vivo studies in young pigs indicate that the GIT is a site of net homocysteine release and thus may contribute to the homocysteinemia. The gut also utilizes 25% of the dietary cysteine intake, and the cysteine uptake by the gut represents approx. 65% of the splanchnic first-pass uptake. Moreover, we recently showed that SAA deficiency significantly suppresses intestinal mucosal growth and reduces intestinal epithelial cell proliferation, and increases intestinal oxidant stress in piglets. These recent findings indicate that intestinal metabolism of dietary methionine and cysteine is nutritionally important for intestinal mucosal growth. Besides their role in protein synthesis, methionine and cysteine are precursors of important molecules. S-adenosylmethionine, a metabolite of methionine, is the principal biological methyl donor in mammalian cells and a precursor for polyamine synthesis. Cysteine is the rate-limiting amino acid for glutathione synthesis, the major cellular antioxidant in mammals. Further studies are warranted to establish how SAA metabolism regulates gut growth and intestinal function, and contributes to the development of gastrointestinal diseases. This review discusses the evidence of SAA metabolism in the GIT and its functional and nutritional importance in gut function and diseases.