The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.

Détails

Ressource 1Télécharger: biomolecules-10-01057.pdf (1562.35 [Ko])
Etat: Public
Version: de l'auteur
Licence: CC BY 4.0
ID Serval
serval:BIB_1E982C7D4533
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.
Périodique
Biomolecules
Auteur(s)
Gausserès B., Liu J., Foppen E., Tourrel-Cuzin C., Rodriguez Sanchez-Archidona A., Delangre E., Cruciani-Guglielmacci C., Pons S., Maskos U., Thorens B., Magnan C., Movassat J., Maouche K.
ISSN
2218-273X (Electronic)
ISSN-L
2218-273X
Statut éditorial
Publié
Date de publication
16/07/2020
Peer-reviewed
Oui
Volume
10
Numéro
7
Pages
1057
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
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.
Mots-clé
Animals, Cell Line, Diabetes Mellitus, Type 2/genetics, Diabetes Mellitus, Type 2/metabolism, Female, Gene Deletion, Glucose/metabolism, Glucose Intolerance/genetics, Glucose Intolerance/metabolism, Hyperglycemia/genetics, Hyperglycemia/metabolism, Insulin Resistance, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, alpha7 Nicotinic Acetylcholine Receptor/genetics, alpha7 Nicotinic Acetylcholine Receptor/metabolism, fat mass, high glycemia, insulin resistance, α7 nAChR, β-cell mass
Pubmed
Web of science
Open Access
Oui
Création de la notice
11/08/2020 11:37
Dernière modification de la notice
24/02/2021 7:24
Données d'usage