Titre
The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Gausserès, B.
Auteure/Auteur
Liu, J.
Auteure/Auteur
Foppen, E.
Auteure/Auteur
Tourrel-Cuzin, C.
Auteure/Auteur
Rodriguez Sanchez-Archidona, A.
Auteure/Auteur
Delangre, E.
Auteure/Auteur
Cruciani-Guglielmacci, C.
Auteure/Auteur
Pons, S.
Auteure/Auteur
Maskos, U.
Auteure/Auteur
Thorens, B.
Auteure/Auteur
Magnan, C.
Auteure/Auteur
Movassat, J.
Auteure/Auteur
Maouche, K.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
2218-273X
Statut éditorial
Publié
Date de publication
2020-07-16
Volume
10
Numéro
7
Première page
1057
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Publication Status: epublish
Résumé
Type 2 diabetes (T2D) occurs by deterioration in pancreatic β-cell function and/or progressive loss of pancreatic β-cell mass under the context of insulin resistance. α7 nicotinic acetylcholine receptor (nAChR) may contribute to insulin sensitivity but its role in the pathogenesis of T2D remains undefined. We investigated whether the systemic lack of α7 nAChR was sufficient to impair glucose homeostasis.
We used an α7 nAChR knock-out (α7 <sup>-/-</sup> ) mouse model fed a standard chow diet. The effects of the lack of α7 nAChR on islet mass, insulin secretion, glucose and insulin tolerance, body composition, and food behaviour were assessed in vivo and ex vivo experiments.
Young α7 <sup>-/-</sup> mice display a chronic mild high glycemia combined with an impaired glucose tolerance and a marked deficit in β-cell mass. In addition to these metabolic disorders, old mice developed adipose tissue inflammation, elevated plasma free fatty acid concentrations and presented glycolytic muscle insulin resistance in old mice. Finally, α7 <sup>-/-</sup> mice, fed a chow diet, exhibited a late-onset excessive gain in body weight through increased fat mass associated with higher food intake.
Our work highlights the important role of α7 nAChR in glucose homeostasis. The constitutive lack of α7 nAChR suggests a novel pathway influencing the pathogenesis of T2D.
We used an α7 nAChR knock-out (α7 <sup>-/-</sup> ) mouse model fed a standard chow diet. The effects of the lack of α7 nAChR on islet mass, insulin secretion, glucose and insulin tolerance, body composition, and food behaviour were assessed in vivo and ex vivo experiments.
Young α7 <sup>-/-</sup> mice display a chronic mild high glycemia combined with an impaired glucose tolerance and a marked deficit in β-cell mass. In addition to these metabolic disorders, old mice developed adipose tissue inflammation, elevated plasma free fatty acid concentrations and presented glycolytic muscle insulin resistance in old mice. Finally, α7 <sup>-/-</sup> mice, fed a chow diet, exhibited a late-onset excessive gain in body weight through increased fat mass associated with higher food intake.
Our work highlights the important role of α7 nAChR in glucose homeostasis. The constitutive lack of α7 nAChR suggests a novel pathway influencing the pathogenesis of T2D.
Sujets
PID Serval
serval:BIB_1E982C7D4533
PMID
Open Access
Oui
Date de création
2020-08-11T09:37:48.111Z
Date de création dans IRIS
2025-05-20T15:47:38Z
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Nom
biomolecules-10-01057.pdf
Version du manuscrit
preprint
Licence
https://creativecommons.org/licenses/by/4.0
Taille
1.53 MB
Format
Adobe PDF
PID Serval
serval:BIB_1E982C7D4533.P001
URN
urn:nbn:ch:serval-BIB_1E982C7D45333
Somme de contrôle
(MD5):21c6ac7135cefc7e88274c613b5da337