Titre :

Glucose Stimulates Gut Motility in Fasted and Fed Conditions: Potential Involvement of a Nitric Oxide Pathway.

Auteur(s) :

Wemelle, Eve [Auteur]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
NeuroMicrobiota
Institut de Recherche en Santé Digestive [IRSD]
Carneiro, Lionel [Auteur]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
NeuroMicrobiota
Institut de Recherche en Santé Digestive [IRSD]
Abot, Anne [Auteur]
Enterosys
Lesage, Jean [Auteur]
Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286
Cani, Patrice D. [Auteur]
Université Catholique de Louvain = Catholic University of Louvain [UCL]
Walloon Excellence in Life sciences and BIOtechnology [Liège] [WELBIO]
NeuroMicrobiota
Knauf, Claude [Auteur]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
Institut de Recherche en Santé Digestive [IRSD]
NeuroMicrobiota

Titre de la revue :

Nutrients

Nom court de la revue :

Nutrients

Numéro :

14

Date de publication :

2022-06-04

ISSN :

2072-6643

Mot(s)-clé(s) en anglais :

type 2 diabetes
glucose transporters
NO
enterosynes
glucose
gut motility

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

(1) Background: Type 2 diabetes (T2D) is associated with a duodenal hypermotility in postprandial conditions that favors hyperglycemia and insulin resistance via the gut-brain axis. Enterosynes, molecules produced within ...
Lire la suite >(1) Background: Type 2 diabetes (T2D) is associated with a duodenal hypermotility in postprandial conditions that favors hyperglycemia and insulin resistance via the gut-brain axis. Enterosynes, molecules produced within the gut with effects on the enteric nervous system, have been recently discovered and pointed to as potential key modulators of the glycemia. Indeed, targeting the enteric nervous system that controls gut motility is now considered as an innovative therapeutic way in T2D to limit intestinal glucose absorption and restore the gut-brain axis to improve insulin sensitivity. So far, little is known about the role of glucose on duodenal contraction in fasted and fed states in normal and diabetic conditions. The aim of the present study was thus to investigate these effects in adult mice. (2) Methods: Gene-expression level of glucose transporters (SGLT-1 and GLUT2) were quantified in the duodenum and jejunum of normal and diabetic mice fed with an HFD. The effect of glucose at different concentrations on duodenal and jejunal motility was studied ex vivo using an isotonic sensor in fasted and fed conditions in both normal chow and HFD mice. (3) Results: Both SGLT1 and GLUT2 expressions were increased in the duodenum (47 and 300%, respectively) and jejunum (75% for GLUT2) of T2D mice. We observed that glucose stimulates intestinal motility in fasted (200%) and fed (400%) control mice via GLUT2 by decreasing enteric nitric oxide release (by 600%), a neurotransmitter that inhibits gut contractions. This effect was not observed in diabetic mice, suggesting that glucose sensing and mechanosensing are altered during T2D. (4) Conclusions: Glucose acts as an enterosyne to control intestinal motility and glucose absorption through the enteric nervous system. Our data demonstrate that GLUT2 and a reduction of NO production could both be involved in this stimulatory contracting effect.Lire moins >

Langue :

Anglais

Comité de lecture :

Oui

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

Université de Lille
Inserm
CHU Lille

Collections :

• Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286

Date de dépôt :

2024-01-12T01:23:44Z
2024-03-08T11:01:57Z