| First Author | Somm E | Year | 2014 |
| Journal | Mol Genet Metab | Volume | 112 |
| Issue | 1 | Pages | 64-72 |
| PubMed ID | 24685552 | Mgi Jnum | J:212123 |
| Mgi Id | MGI:5578098 | Doi | 10.1016/j.ymgme.2014.03.003 |
| Citation | Somm E, et al. (2014) Concomitant alpha7 and beta2 nicotinic AChR subunit deficiency leads to impaired energy homeostasis and increased physical activity in mice. Mol Genet Metab 112(1):64-72 |
| abstractText | Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated cation channels well characterized in neuronal signal transmission. Moreover, recent studies have revealed nAChR expression in nonneuronal cell types throughout the body, including tissues involved in metabolism. In the present study, we screen gene expression of nAChR subunits in pancreatic islets and adipose tissues. Mice pancreatic islets present predominant expression of alpha7 and beta2 nAChR subunits but at a lower level than in central structures. Characterization of glucose and energy homeostasis in alpha7beta2nAChR(-/-) mice revealed no major defect in insulin secretion and sensitivity but decreased glycemia apparently unrelated to gluconeogenesis or glycogenolysis. alpha7beta2nAChR(-/-) mice presented an increase in lean and bone body mass and a decrease in fat storage with normal body weight. These observations were associated with elevated spontaneous physical activity in alpha7beta2nAChR(-/-) mice, mainly due to elevation in fine vertical (rearing) activity while their horizontal (ambulatory) activity remained unchanged. In contrast to alpha7nAChR(-/-) mice presenting glucose intolerance and insulin resistance associated to excessive inflammation of adipose tissue, the present metabolic phenotyping of alpha7beta2nAChR(-/-) mice revealed a metabolic improvement possibly linked to the increase in spontaneous physical activity related to central beta2nAChR deficiency. |
