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© Uwe Maskos
Tranche d'hippocampe de souris colorée avec deux toxines spécifiques de sous-types de récepteur nicotinique, en rouge (grains), et en vert (corps cellulaires). L'hippocampe est la zone du cerveau qui gère la mémoire spatiale.
Publication : Biomolecules

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Biomolecules - 16 Jul 2020

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,

Link to Pubmed [PMID] – 32708537

Link to DOI [DOI] – E105710.3390/biom10071057

Biomolecules 2020 07; 10(7):

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-/-) 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-/- 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-/- 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.

https://pubmed.ncbi.nlm.nih.gov/32708537