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Dietary fibre (and animal products) modulate the association between tryptophan intake, gut microbiota and type 2 diabetes: but how?
  1. Lin Shi1,
  2. Rikard Landberg2
  1. 1College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an, Shaanxi, China
  2. 2Department of Life Sciences, Chalmers University of Technology, Gothenburg, Sweden
  1. Correspondence to Professor Rikard Landberg, Department of LifeSciences, Chalmers University of Technology, Gothenburg, SE-41296, Sweden; rikard.landberg{at}

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There is an increased interest in the interplay among diet, gut microbiota and health. Studies have often investigated the influence of diets, foods and dietary components on gut microbiota or whether microbiota can modify the effect of dietary interventions and the role of such modifications on health outcomes.1 This has been fueled by promising results emerging from large landmark studies pinpointing the role of gut microbiota as an important determinant for metabolic responses and from an improved understanding of how gut microbiota affect metabolism and how it mediate effects through generation of metabolites.1–3 The faecal metabolome has shown to explain up to 60% variability in gut microbial composition, some of them are key mediators of physiological effects directly produced or modified by gut microbiota such as bile acids, short-chain fatty acids, lipopolysaccharides and trimethylamine N-oxide.3 The concentrations of these compounds are determined by the interaction between specific microbiota functionalities and diet components.2 3

Indolepropionate (IPA), a microbial metabolite of the essential amino acid—tryptophan, represents a recent addition to the family of gut microbial metabolites that emerge from such interactions. Around 95% of tryptophan consumed is catabolised through the host kynurenine pathway in the liver and peripheral tissues, but a small, yet important, fraction is directly used by gut microbiota to produce indole and its derivatives, such as …

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  • Contributors Both authors designed and wrote the commentary.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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