The impact of dietary fermentable carbohydrates on a postinflammatory model of irritable bowel syndrome

Tuck CJ1, Caminero A2, Jiménez Vargas NN1, Soltys CL1, Jaramillo Polanco JO1, Lopez Lopez CD1, Constante M2, Lourenssen SR1, Verdu EF2, Muir JG3, Lomax AE1, Reed DE1, Vanner SJ1. Neurogastroenterol Motil. 2019 Jul 9:e13675. doi: 10.1111/nmo.13675. [Epub ahead of print]


Author information

Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada.

Farncombe Institute, McMaster University, Hamilton, Ontario, Canada.

Department of Gastroenterology, Monash University, Melbourne, Victoria, Australia.


BACKGROUND: A low fermentable carbohydrate (FODMAP) diet is used in quiescent inflammatory bowel disease when irritable bowel syndrome-like symptoms occur. There is concern that the diet could exacerbate inflammation by modifying microbiota and short-chain fatty acid (SCFA) production. We examined the effect of altering dietary FODMAP content on inflammation in preclinical inflammatory models.

METHODS: C57BL/6 mice were given 3% dextran sodium sulfate (DSS) in drinking water for 5 days and recovered for 3 weeks (postinflammatory, n = 12), or 5 days (positive-control, n = 12). Following recovery, DSS-treated or control mice (negative-control, n = 12) were randomized to 2-week low- (0.51 g/100 g total FODMAP) or high-FODMAP (4.10 g) diets. Diets mimicked human consumption containing fructose, sorbitol, galacto-oligosaccharide, and fructan. Colons were assessed for myeloperoxidase (MPO) activity and histological damage. Supernatants were generated for perforated patch-clamp recordings and cytokine measurement. Cecum contents were analyzed for microbiota, SCFA, and branched-chain fatty acids (BCFA). Data were analyzed by two-way ANOVA with Bonferroni.

KEY RESULTS: Inflammatory markers were higher in the positive-control compared with negative-control and postinflammatory groups, but no differences occurred between the two diets within each treatment (MPO P > .99, histological scores P > .99, cytokines P > .05), or the perforated patch-clamp recordings (P > .05). Microbiota clustered mainly based on DSS exposure. No difference in SCFA content occurred. Higher total BCFA occurred with the low-FODMAP diet in positive-control (P < .01) and postinflammatory groups (P < .01).

CONCLUSIONS AND INFERENCES: In this preclinical study, reducing dietary FODMAPs did not exacerbate nor mitigate inflammation. Microbiota profile changes were largely driven by inflammation rather than diet. Low FODMAP intake caused a shift toward proteolytic fermentation following inflammation.

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