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

Abstract

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. C57BL/6 mice were given 3% dextran sodium sulfate (DSS) in drinking water for 5days and recovered for 3weeks (postinflammatory, n=12), or 5days (positive-control, n=12). Following recovery, DSS-treated or control mice (negative-control, n=12) were randomized to 2-week low- (0.51g/100g total FODMAP) or high-FODMAP (4.10g) 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. 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). 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.