| First Author | Dezfuli G | Year | 2020 |
| Journal | Neuropharmacology | Volume | 166 |
| Pages | 107921 | PubMed ID | 31881170 |
| Mgi Jnum | J:304657 | Mgi Id | MGI:6693914 |
| Doi | 10.1016/j.neuropharm.2019.107921 | Citation | Dezfuli G, et al. (2020) alpha4beta2 nicotinic acetylcholine receptors intrinsically influence body weight in mice. Neuropharmacology 166:107921 |
| abstractText | Desensitization of the nicotinic acetylcholine receptor (nAChR) containing the beta2 subunit is a potentially critical mechanism underlying the body weight (BW) reducing effects of nicotine. The purpose of this study was a) to determine the alpha subunit(s) that partners with the beta2 subunit to form the nAChR subtype that endogenously regulates energy balance and b) to probe the extent to which nAChR desensitization could be involved in the regulation of BW. We demonstrate that deletion of either the alpha4 or the beta2, but not the alpha5, subunit of the nAChR suppresses weight gain in a sex-dependent manner. Furthermore, chronic treatment with the beta2-selective nAChR competitive antagonist dihydro-beta-erythroidine (DHbetaE) in mice fed a high-fat diet suppresses weight gain. These results indicate that heteromeric alpha4beta2 nAChRs play a role as intrinsic regulators of energy balance and that desensitizing or inhibiting this nAChR is likely a relevant mechanism and thus could be a strategy for weight loss. |
