Complementary intestinal mucosa and microbiota responses to caloric restriction.

Détails

Ressource 1Télécharger: s41598-018-29815-7.pdf (4273.72 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_6A012BFDB686
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Complementary intestinal mucosa and microbiota responses to caloric restriction.
Périodique
Scientific Reports
Auteur(s)
Duszka K., Ellero-Simatos S., Ow G.S., Defernez M., Paramalingam E., Tett A., Ying S., König J., Narbad A., Kuznetsov V.A., Guillou H., Wahli W.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Statut éditorial
Publié
Date de publication
2018
Peer-reviewed
Oui
Volume
8
Numéro
1
Pages
11338
Langue
anglais
Résumé
The intestine is key for nutrient absorption and for interactions between the microbiota and its host. Therefore, the intestinal response to caloric restriction (CR) is thought to be more complex than that of any other organ. Submitting mice to 25% CR during 14 days induced a polarization of duodenum mucosa cell gene expression characterised by upregulation, and downregulation of the metabolic and immune/inflammatory pathways, respectively. The HNF, PPAR, STAT, and IRF families of transcription factors, particularly the Pparα and Isgf3 genes, were identified as potentially critical players in these processes. The impact of CR on metabolic genes in intestinal mucosa was mimicked by inhibition of the mTOR pathway. Furthermore, multiple duodenum and faecal metabolites were altered in CR mice. These changes were dependent on microbiota and their magnitude corresponded to microbial density. Further experiments using mice with depleted gut bacteria and CR-specific microbiota transfer showed that the gene expression polarization observed in the mucosa of CR mice is independent of the microbiota and its metabolites. The holistic interdisciplinary approach that we applied allowed us to characterize various regulatory aspects of the host and microbiota response to CR.
Pubmed
Web of science
Open Access
Oui
Création de la notice
15/08/2018 8:27
Dernière modification de la notice
20/08/2019 15:24
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