Background: Mucosal healing (MH) decreases the relapse risk in patients with inflammatory bowel disease, but the role of dietary supplementation in this process has been poorly investigated. Here, we investigated the effect of an amino acid mixture supplement on rat MH.
Methods: Colitis was induced using 5% of dextran sodium sulfate for 6 days. Then, rats received a mixture of threonine (0.50 g/d), methionine (0.31 g/d), and monosodium glutamate (0.57 g/d) or an isonitrogenous amount of alanine (control group). Colons were recovered after colitis induction and after dietary supplementation for measuring colon characteristics, myeloperoxidase, cytokine gene expression, glutathione content, protein synthesis rate, and for histological analysis. Short-chain fatty acids were measured in the colonic content.
Results: Colitis induction resulted in anorexia, thickening and shortening of the colon, and ulceration. Colonic cytokine expression and neutrophil infiltration were increased. An increased amount of water and a decreased amount of butyrate, propionate, and acetate were measured in the colonic content. Supplementation with the amino acid mixture coincided with a reduced protein synthesis rate in the colon compatible with the observed increased colonic MH. Mucosal regeneration/re-epithelialization was visible within 3 days after colitis induction at a time when mucosal inflammation was severe. Histological analysis revealed an increased regeneration/re-epithelialization after 10-day supplementation. In contrast, the spontaneous resolution of inflammation was not affected by the supplementation.
Conclusions: Amino acid supplementation ameliorates colonic MH but not mucosal inflammatory status. Our data sustain the use of adjuvant dietary intervention on initiated intestinal MH.
Article first published online 4 November 2013
*UMR 914 PNCA INRA, AgroParisTech Physiologie de la Nutrition et du Comportement Alimentaire, Paris, France;
†Service d’Anatomie et Cytologie Pathologique, Hôpital Xavier Bichat, Paris, France;
‡INSERM U773, Centre de Recherche Biomédicale Bichat Beaujon/Université Paris 7, Paris, France;
§Frontier Research Laboratory, Institute for Innovation, Ajinomoto Co. Inc., Kawasaki, Japan; and
‖Departement de Gastroentérologie, Hôpital Avicenne, Assistance Publique-Hôpitaux de Paris, Bobigny, France.
Reprints: François Blachier, PhD, UMR 914 PNCA INRA, AgroParisTech Physiologie de la Nutrition et du Comportement Alimentaire, 16 Rue Claude Bernard, Paris 75005, France (e-mail: firstname.lastname@example.org).
The authors have no conflicts of interest to disclose.
Received August 29, 2013
Accepted September 18, 2013