| First Author | Gausserès B | Year | 2020 |
| Journal | Biomolecules | Volume | 10 |
| Issue | 7 | PubMed ID | 32708537 |
| Mgi Jnum | J:302364 | Mgi Id | MGI:6508211 |
| Doi | 10.3390/biom10071057 | Citation | Gausseres B, et al. (2020) The Constitutive Lack of alpha7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse. Biomolecules 10(7):1057 |
| abstractText | OBJECTIVE: Type 2 diabetes (T2D) occurs by deterioration in pancreatic beta-cell function and/or progressive loss of pancreatic beta-cell mass under the context of insulin resistance. alpha7 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 alpha7 nAChR was sufficient to impair glucose homeostasis. METHODS: We used an alpha7 nAChR knock-out (alpha7(-/-)) mouse model fed a standard chow diet. The effects of the lack of alpha7 nAChR on islet mass, insulin secretion, glucose and insulin tolerance, body composition, and food behaviour were assessed in vivo and ex vivo experiments. RESULTS: Young alpha7(-/-) mice display a chronic mild high glycemia combined with an impaired glucose tolerance and a marked deficit in beta-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, alpha7(-/-) mice, fed a chow diet, exhibited a late-onset excessive gain in body weight through increased fat mass associated with higher food intake. CONCLUSION: Our work highlights the important role of alpha7 nAChR in glucose homeostasis. The constitutive lack of alpha7 nAChR suggests a novel pathway influencing the pathogenesis of T2D. |
