Gut commensal E. coli proteins activate host satiety pathways following nutrient-induced bacterial growth

Jonathan Brenton, Naouel Tennoune, Nicolas Lucas, Marie Francois, Romain Legrand, Justine Jacquemot, Alexis Goichon, Charlene Guerin, Johann Peltier, Martine Pestel-Caron, Philippe Chan, David Vaudry, Jean-Claude do Rego, Fabienne Lienard, Luc Penicaud, Xavier Fioramonti, Ivor Ebenezer, Tomas Hokfelt, Pierre Dechelotte, Serguei Fetissov

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The composition of gut microbiota has been associated with host metabolic phenotypes, but it is not known if gut bacteria may influence host appetite. Here we show that regular nutrient provision stabilizes exponential growth of E. coli, with the stationary phase occurring 20 min after nutrient supply accompanied by bacterial proteome changes, suggesting involvement of bacterial proteins in host satiety. Indeed, intestinal infusions of E. coli stationary phase proteins increased plasma PYY and their intraperitoneal injections suppressed acutely food intake and activated c-Fos in hypothalamic POMC neurons, while their repeated administrations reduced meal size. ClpB, a bacterial protein mimetic of α-MSH, was upregulated in the E. coli stationary phase, was detected in plasma proportional to ClpB DNA in feces, and stimulated firing rate of hypothalamic POMC neurons. Thus, these data show that bacterial proteins produced after nutrient-induced E. coli growth may signal meal termination. Furthermore, continuous exposure to E. coli proteins may influence long-term meal pattern.
Original languageEnglish
Pages (from-to)324-334
JournalCell Metabolism
Early online date24 Nov 2015
Publication statusPublished - 9 Feb 2016


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