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Research Project: MOLECULAR, CELLULAR, AND REGULATORY ASPECTS OF OBESITY DEVELOPMENT IN CHILDREN

Location: Children's Nutrition Research Center

Title: New insights into sulfur amino acids function in gut health and disease

Author
item Burrin, Douglas - Doug
item Stoll, Barbara - Children's Nutrition Research Center (CNRC)
item Benight, Nancy - Children's Nutrition Research Center (CNRC)
item Bauchart-thevret, Caroline - Children's Nutrition Research Center (CNRC)

Submitted to: Amino Acids
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/2013
Publication Date: 10/5/2013
Citation: Burrin, D.G., Stoll, B., Benight, N., Bauchart-Thevret, C. 2013. New insights into sulfur amino acids function in gut health and disease. Amino Acids. 45:597-598.

Interpretive Summary:

Technical Abstract: The gastrointestinal tract (GIT) is a metabolically significant site of sulfur amino acids (SAAs) metabolism in the body. Aside from their role in protein synthesis, methionine and cysteine are involved in many biological functions and diseases. Methionine (MET) is an indispensable amino acid and is transmethylated to homocysteine via S-adenosylmethionine (SAM), the principal biological methyl donor in mammalian cells and a precursor for polyamine synthesis. We have examined the role of SAA metabolism in GIT health and disease. Our studies in young pigs showed that the whole-body methionine transmethylation and remethylation rates were higher during duodenal [(13)C]-MET than intravenous [(2)H[3]]-MET infusion. Thus, transmethylation and transsulfuration in the GIT represented 27% and 23% of whole-body fluxes, respectively. Additional studies show how disruption of methionine cycle activity and dietary supplementation with methionine metabolites affects the susceptibility to colitis in mice. We found that mice fed vitamin B[12]/B[6] deficient diets are protected against colitis with reduced inflammation and tissue injury. We also found that B-vitamin deficiency suppressed inflammatory gene expression in association with altered MET cycle activity and indices of methylation status. We also showed that supplementation with the MET cycle metabolite, methylthioadenosine (MTA), prevented inflammation during colitis in mice. These results suggest that MTA also is protective against experimental colitis and reduced tissue injury and expression of multiple inflammatory genes. The presentation will discuss the evidence of sulfur amino acid metabolism in GIT and consequences of MET cycle activity in health and disease.