Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth
Open accessAbstract
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.
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A separate study in rodents demonstrated that bacterial proteins produced after nutrient-induced Escherichia coli growth may signal the CNS via increased plasma PYY.
“A separate study in rodents demonstrated that bacterial proteins produced after nutrient-induced Esherichia coli growth may signal the CNS via increased plasma PYY [205].”
From Anxiety, depression, and the microbiome: A role for gut peptides (2018) · cites this paper as [205]
Autoantibody-induced interference with the central melanocortin system is one of the key microbiota-gut-brain mechanisms contributing to dysregulated appetite control in eating disorders.
“Finally, data on the bacterial protein C1pB (produced by both commensal and pathogenic microorganisms) as a mimetic of α-MSH and its effects on activating host satiety pathways in rodents [47], as well as the elevated plasma concentration of anti-C1pB IgG that is cross-reactive with α-MSH in patients with eating disorders [48], accord with the notion that autoantibody-induced interference with the”
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- Authors
- Breton, J., Tennoune, N., Lucas, N., Francois, M., Legrand, R., Jacquemot, J., Goichon, A., Guérin, C., Peltier, J., Pestel-Caron, M., Chan, P., Vaudry, D., do Rego, J.-C., Liénard, F., Pénicaud, L., Fioramonti, X., Ebenezer, I. S., Hökfelt, T., Déchelotte, P., & Fetissov, S. O.
- Affiliations
- Inserm (FR)
- Institute for Research and Innovation in Biomedicine (FR)
- Centre National de la Recherche Scientifique (FR)
- University of Portsmouth (GB)
- Karolinska Institutet (SE)
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2016-02
- Volume
- 23
- Issue
- 2
- Pages
- 324-334
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2174651366
- Cited by
- 321
- References
- 53
- Citations by year
- 2026: 18 · 2025: 33 · 2024: 27 · 2023: 30 · 2022: 30 · 2021: 37 · 2020: 26 · 2019: 32 · 2018: 34 · 2017: 26 · 2016: 27 · 2015: 1
- FWCI
- 16.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Région Normandie
- Interreg
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- gut commensal bacteria, Escherichia coli, bacterial proteins, satiety, appetite regulation, dietary intake, peptide YY, ClpB, POMC neurons, hypothalamus, bacterial growth phase, stationary phase, meal termination, meal size, gut microbiota, host-microbe signaling
- MeSH terms
- Adenosine Triphosphate, Amygdala, Animals, Escherichia coli, Feeding Behavior, Female, Heat-Shock Proteins, Hypothalamus, Male, Mice, Inbred C57BL, Neurons, Pro-Opiomelanocortin, Satiety Response, Proto-Oncogene Proteins c-fos, Rats, Sprague-Dawley, Rats, Wistar, Peptide YY, Escherichia coli Proteins, Proteomics, Gastrointestinal Tract, Endopeptidase Clp, Mice, Glucagon-Like Peptide 1, Electrophysiological Phenomena
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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