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

Neurogastroenterol Motil. 2019 Oct;31(10):e13675. doi: 10.1111/nmo.13675. Epub 2019 Jul 9.

Abstract

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.

Keywords: di-; dietary therapy; fermentable oligo-; fermentation patterns; inflammation; mono-saccharides and polyols.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / metabolism
  • Colitis / pathology
  • Cytokines / metabolism
  • Dextran Sulfate / toxicity
  • Dietary Carbohydrates*
  • Disaccharides
  • Disease Models, Animal
  • Fatty Acids / metabolism*
  • Fatty Acids, Volatile / metabolism*
  • Fermentation*
  • Gastrointestinal Microbiome / genetics*
  • Hemiterpenes / metabolism
  • Inflammation
  • Inflammatory Bowel Diseases / metabolism
  • Inflammatory Bowel Diseases / pathology
  • Irritable Bowel Syndrome / diet therapy*
  • Irritable Bowel Syndrome / metabolism
  • Irritable Bowel Syndrome / microbiology
  • Irritable Bowel Syndrome / pathology
  • Isobutyrates / metabolism
  • Mice
  • Monosaccharides
  • Nociception
  • Oligosaccharides
  • Patch-Clamp Techniques
  • Pentanoic Acids / metabolism
  • Peroxidase / metabolism*
  • RNA, Ribosomal, 16S

Substances

  • Cytokines
  • Dietary Carbohydrates
  • Disaccharides
  • Fatty Acids
  • Fatty Acids, Volatile
  • Hemiterpenes
  • Isobutyrates
  • Monosaccharides
  • Oligosaccharides
  • Pentanoic Acids
  • RNA, Ribosomal, 16S
  • isovaleric acid
  • isobutyric acid
  • Dextran Sulfate
  • Peroxidase