Authors: Antonio Molinaro, Pierre Bel Lassen, Marcus Henricsson, Hao Wu, Solia Adriouch, Eugeni Belda, Rima Chakaroun, Trine Nielsen, Per-Olof Bergh, Christine Rouault, Sébastien André, Florian Marquet, Fabrizio Andreelli, Joe-Elie Salem, Karen Assmann, Jean-Philippe Bastard, Sofia Forslund, Emmanuelle Le Chatelier, Gwen Falony, Nicolas Pons, Edi Prifti, Benoit Quinquis, Hugo Roume, Sara Vieira-Silva, Tue H. Hansen, Helle Krogh Pedersen, Christian Lewinter, Nadja B. Sønderskov, The MetaCardis Consortium, Lars Køber, Henrik Vestergaard, Torben Hansen, Jean-Daniel Zucker, Pilar Galan, Marc-Emmanuel Dumas, Jeroen Raes, Jean-Michel Oppert, Ivica Letunic, Jens Nielsen, Peer Bork, S. Dusko Ehrlich, Michael Stumvoll, Oluf Pedersen, Judith Aron-Wisneswky, Karine Clément & Fredrik Bäckhed.
Nat Commun 11, 5881 (2020).
PubMed ID: Not yet


Abstract: Microbiota-host-diet interactions contribute to the development of metabolic diseases. Imidazole propionate is a novel microbially produced metabolite from histidine, which impairs glucose metabolism. Here, we show that subjects with prediabetes and diabetes in the MetaCardis cohort from three European countries have elevated serum imidazole propionate levels. Furthermore, imidazole propionate levels were increased in subjects with low bacterial gene richness and Bacteroides 2 enterotype, which have previously been associated with obesity. The Bacteroides 2 enterotype was also associated with increased abundance of the genes involved in imidazole propionate biosynthesis from dietary histidine. Since patients and controls did not differ in their histidine dietary intake, the elevated levels of imidazole propionate in type 2 diabetes likely reflects altered microbial metabolism of histidine, rather than histidine intake per se. Thus the microbiota may contribute to type 2 diabetes by generating imidazole propionate that can modulate host inflammation and metabolism.