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Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth.
- Source :
-
Cell metabolism [Cell Metab] 2016 Feb 09; Vol. 23 (2), pp. 324-34. Date of Electronic Publication: 2015 Nov 24. - Publication Year :
- 2016
-
Abstract
- 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.<br /> (Copyright © 2016 Elsevier Inc. All rights reserved.)
- Subjects :
- Adenosine Triphosphate biosynthesis
Amygdala metabolism
Animals
Electrophysiological Phenomena
Endopeptidase Clp
Escherichia coli metabolism
Feeding Behavior
Female
Glucagon-Like Peptide 1 metabolism
Heat-Shock Proteins metabolism
Hypothalamus metabolism
Male
Mice
Mice, Inbred C57BL
Neurons metabolism
Peptide YY metabolism
Pro-Opiomelanocortin metabolism
Proteomics
Proto-Oncogene Proteins c-fos metabolism
Rats, Sprague-Dawley
Rats, Wistar
Escherichia coli growth & development
Escherichia coli Proteins metabolism
Gastrointestinal Tract microbiology
Satiety Response
Subjects
Details
- Language :
- English
- ISSN :
- 1932-7420
- Volume :
- 23
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cell metabolism
- Publication Type :
- Academic Journal
- Accession number :
- 26621107
- Full Text :
- https://doi.org/10.1016/j.cmet.2015.10.017