Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth
Cell Metabolism. 2016-02-01; 23(2): 324-334
DOI: 10.1016/j.cmet.2015.10.017
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1. Cell Metab. 2016 Feb 9;23(2):324-34. doi: 10.1016/j.cmet.2015.10.017. Epub
2015 Nov 24.
Gut Commensal E. coli Proteins Activate Host Satiety Pathways following
Nutrient-Induced Bacterial Growth.
Breton J(1), Tennoune N(1), Lucas N(1), Francois M(1), Legrand R(1), Jacquemot
J(1), Goichon A(1), Guérin C(1), Peltier J(2), Pestel-Caron M(3), Chan P(4),
Vaudry D(4), do Rego JC(5), Liénard F(6), Pénicaud L(6), Fioramonti X(6),
Ebenezer IS(7), Hökfelt T(8), Déchelotte P(9), Fetissov SO(10).
Author information:
(1)Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen 76183, France;
Institute for Research and Innovation in Biomedicine (IRIB), Rouen University,
Normandy University, Rouen 76000, France.
(2)Microbiology Laboratory GRAM, EA2656, Rouen 76183, France; Institute for
Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy
University, Rouen 76000, France.
(3)Microbiology Laboratory GRAM, EA2656, Rouen 76183, France; Institute for
Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy
University, Rouen 76000, France; Rouen University Hospital, CHU Charles Nicolle,
Rouen 76183, France.
(4)PISSARO Proteomic Platform, Mont-Saint-Aignan 76821, France; Institute for
Research and Innovation in Biomedicine (IRIB), Rouen University, Normandy
University, Rouen 76000, France.
(5)Animal Behavior Platform (SCAC), Rouen 76183, France; Institute for Research
and Innovation in Biomedicine (IRIB), Rouen University, Normandy University,
Rouen 76000, France.
(6)Centre for Taste and Feeding Behaviour, UMR 6265-CNRS, 1324-INRA, Bourgogne
Franche Comté University, Dijon F 21000, France.
(7)Neuropharmacology Research Group, School of Pharmacy and Biomedical Sciences
University of Portsmouth, Portsmouth PO 1 2DT, UK.
(8)Department of Neuroscience, Karolinska Institutet, Stockholm 17176, Sweden.
(9)Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen 76183, France;
Institute for Research and Innovation in Biomedicine (IRIB), Rouen University,
Normandy University, Rouen 76000, France; Rouen University Hospital, CHU Charles
Nicolle, Rouen 76183, France.
(10)Inserm UMR1073, Nutrition, Gut and Brain Laboratory, Rouen 76183, France;
Institute for Research and Innovation in Biomedicine (IRIB), Rouen University,
Normandy University, Rouen 76000, France. Electronic address:
.
Comment in
Nat Rev Endocrinol. 2016 Jan;12(1):4. doi: 10.1038/nrendo.2015.213.
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.
Copyright © 2016 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.cmet.2015.10.017
PMID: 26621107 [Indexed for MEDLINE]