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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #243693

Title: The role of methionine metabolism in inflammatory bowel disease

item Benight, Nancy
item Stoll, Barbara
item Puiman, Patrycja
item Burrin, Douglas - Doug

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 4/1/2009
Publication Date: 5/1/2009
Publication URL:
Citation: Benight, N.M., Stoll, B., Puiman, P., Burrin, D. 2009. The role of methionine metabolism in inflammatory bowel disease [abstract]. Journal of Federation of American Societies for Experimental Biology. 23:919.6

Interpretive Summary:

Technical Abstract: Methionine (Met) cycle activity is critical for normal cell functions. Met metabolites S-adenosylmethionine (SAM) and methylthioadenosine (MTA) are anti-inflammatory, yet their role in inflammatory bowel disease (IBD) is poorly understood. We hypothesize that active IBD leads to changes in Met metabolites that impact disease and administration of SAM and MTA will reduce inflammation. Study 1 mice received either a control diet (C) or a B6/B12-deficient diet (D) to disrupt Met metabolism. Mice in both groups were challenged with dextran sulfate sodium (DSS) at 5% acutely or 2.5% chronically. Study 2 mice fed the C diet were then pretreated with control, SAM or MTA supplemented water for 7 days. During days 3-7, all mice were received 3% DSS. We measured weight change, clinical disease activity index (DAI) and collected colon for analysis in both studies. Study 1 mice fed the C diet had a higher mortality rate of 87.5% after 5% DSS when compared to D diet fed mice 37.5%. Similar results were seen with the 2.5% DSS (25% in C vs. 0% in D) and D diet fed mice had reduction in DAI compared to C fed mice. In Study 2, the MTA group had lower DAI and weight loss. No difference was detected in molecular markers or histology in either study. Met cycle disruption via B-vitamin deficiency and supplementing MTA were protective during colitis. We postulate that Met metabolites are modulating colonic inflammation.