M Shinozaki1, H Saito, T Muto. 1. Department of Surgery, Faculty of Medicine, University of Tokyo, Japan.
Abstract
BACKGROUND: Although the pathogenesis of Crohn's disease remains unclear, an elemental diet has been shown to be clinically effective. Glutamine is an energy source for many cell types including colonocytes. PURPOSE: This study was designed to assess the potential clinical effects on colitis of changing the dietary quantity of glutamine. METHODS: Colitis was induced by intrarectal administration of 30 mg of trinitrobenzenesulfonic acid with 50 percent ethanol vehicle in Sprague-Dawley rats. Rats were randomly allocated into three dietary groups: Group 1, a commercial elemental diet-based diet without glutamine; Group 2, a commercial elemental diet (glutamine: 12 percent of amino acid content); Group 3, elemental diet with 24 percent glutamine. Diets were started one week before colitis induction and continued until sacrifice. Rats were killed at one, three, and five weeks after colitis induction, and colons were excised. Damage evaluation was based on the percentage of rats with ulcer, macroscopic damage score, average ulcer area, and microscopic damage score. RESULTS: Group 2 rats weighed more than Group 1 rats at three weeks because of their higher dietary intake. At one week after colitis induction, all groups had comparable damage. At three weeks, the macroscopic damage score was higher in Group 3 than in Groups 1 and 2. At five weeks, rats in Group 3 had significantly more severe damage than those in Groups 1 and 2 in terms of all four indexes. CONCLUSION: We conclude that excess glutamine has a deleterious effect on ulcers in trinitrobenzenesulfonic acid-induced colitis.
BACKGROUND: Although the pathogenesis of Crohn's disease remains unclear, an elemental diet has been shown to be clinically effective. Glutamine is an energy source for many cell types including colonocytes. PURPOSE: This study was designed to assess the potential clinical effects on colitis of changing the dietary quantity of glutamine. METHODS:Colitis was induced by intrarectal administration of 30 mg of trinitrobenzenesulfonic acid with 50 percent ethanol vehicle in Sprague-Dawley rats. Rats were randomly allocated into three dietary groups: Group 1, a commercial elemental diet-based diet without glutamine; Group 2, a commercial elemental diet (glutamine: 12 percent of amino acid content); Group 3, elemental diet with 24 percent glutamine. Diets were started one week before colitis induction and continued until sacrifice. Rats were killed at one, three, and five weeks after colitis induction, and colons were excised. Damage evaluation was based on the percentage of rats with ulcer, macroscopic damage score, average ulcer area, and microscopic damage score. RESULTS: Group 2 rats weighed more than Group 1 rats at three weeks because of their higher dietary intake. At one week after colitis induction, all groups had comparable damage. At three weeks, the macroscopic damage score was higher in Group 3 than in Groups 1 and 2. At five weeks, rats in Group 3 had significantly more severe damage than those in Groups 1 and 2 in terms of all four indexes. CONCLUSION: We conclude that excess glutamine has a deleterious effect on ulcers in trinitrobenzenesulfonic acid-induced colitis.