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ObjectiveUlcerative colitis is a chronic recurrent disease characterized by acute inflammation of the colonic mucosa. In Japan, a dietary supplementation product enriched with glutamine, dietary fiber, and oligosaccharide (GFO) is widely applied for enteral nutrition support. These three components have been suggested to improve intestinal health. In this study, we investigated whether GFO has suppressive effects on mucosal damage in ulcerative colitis in an experimental mouse model.MethodsC57BL/6 mice received 2.5% dextran sulfate sodium in drinking water for 5 d to induce colitis. Then, they were given 0.25 mL of GFO or a 20% glucose solution twice daily for 10 d. Another set of mice receiving unaltered drinking water was used as the normal control group.ResultsThe body weight loss and disease activity index were significantly lower in the GFO-treated mice compared with the glucose-treated mice (P < 0.05). The decrease in colon length induced by dextran sulfate sodium was significantly alleviated in GFO-treated mice compared with glucose-treated mice (P < 0.01). In addition, the histologic findings showed that intestinal inflammation was significantly attenuated in mice treated with GFO. Furthermore, treatment with GFO significantly inhibited the dextran sulfate sodium-induced increase in the mRNA expression of interleukin-1β.ConclusionThese results suggest that GFO has potential therapeutic value as an adjunct therapy for ulcerative colitis.

Original publication

DOI

10.1016/j.nut.2012.09.007

Type

Journal article

Journal

Nutrition (Burbank, Los Angeles County, Calif.)

Publication Date

03/2013

Volume

29

Pages

549 - 555

Addresses

Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.

Keywords

Intestinal Mucosa, Colon, Animals, Mice, Inbred C57BL, Mice, Colitis, Ulcerative, Disease Models, Animal, Dextran Sulfate, Oligosaccharides, Glutamine, RNA, Messenger, Cytokines, Enteral Nutrition, Dietary Fiber, Dietary Supplements, Male, Interleukin-1beta