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. 2020 Dec 3;70(6):1174–1182. doi: 10.1136/gutjnl-2020-323071

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Tryptophan metabolism alterations in metabolic syndrome. Tryptophan dysmetabolism is associated with liver inflammation, steatosis and insulin resistance. In metabolic syndrome (MetS), the inflammatory state is associated with kynurenine (KYN) production through the activation of indoleamine 2,3-dioxygenase 1 (IDO1). This leads to an increase in kynurenine-derived metabolites, such as kynurenic acid (KYNA), xanthurenic acid (XA), 3-hydroxykynurenine (3-H-KYN), 3-hydroxyanthranilic acid (3-HAA) and quinolinic acid (QA). In parallel, the gut microbiota presents a defect in the production of aryl hydrocarbon receptor (AhR) ligands such as indole-3-propionic acid (IPA). The incretin hormone glucagon-like peptide 1 (GLP-1) secretion from intestinal enteroendocrine L cells and interleukin (IL)-22 production are decreased, altering gut permeability and promoting lipopolysaccharide (LPS) translocation. Serotonin (5-HT) biosynthesis from intestinal enterochromaffin cells is also reduced in the context of MetS due to a decrease in the production of microbiota-derived metabolites inducing the production of host 5-HT.