The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.
fat mass
high glycemia
insulin resistance
α7 nAChR
β-cell mass
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
16 07 2020
16 07 2020
Historique:
received:
04
05
2020
revised:
03
07
2020
accepted:
13
07
2020
entrez:
26
7
2020
pubmed:
28
7
2020
medline:
10
2
2021
Statut:
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 Young α7 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.
Identifiants
pubmed: 32708537
pii: biom10071057
doi: 10.3390/biom10071057
pmc: PMC7408520
pii:
doi:
Substances chimiques
alpha7 Nicotinic Acetylcholine Receptor
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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