| First Author | Breum AW | Year | 2022 |
| Journal | Endocrinology | Volume | 163 |
| Issue | 7 | PubMed ID | 35595472 |
| Mgi Jnum | J:326875 | Mgi Id | MGI:7314557 |
| Doi | 10.1210/endocr/bqac079 | Citation | Breum AW, et al. (2022) Divergent Roles of alpha5 and beta4 Nicotinic Receptor Subunits in Food Reward and Nicotine-induced Weight Loss in Male Mice. Endocrinology 163(7) |
| abstractText | A major obstacle to successful smoking cessation is the prospect of weight gain. Despite a clear relationship between cigarette smoking and body weight, surprisingly little is known about the physiological and molecular mechanism by which nicotine affects energy homeostasis and food-motivated behaviors. Here we use loss-of-function mouse models to demonstrate that 2 nicotinic acetylcholine receptor (nAChR) subunits encoded by the CHRNA5-CHRNA3-CHRNB4 gene cluster, alpha5 and beta4, exhibit divergent roles in food reward. We also reveal that beta4-containing nAChRs are essential for the weight-lowering effects of nicotine in diet-induced obese mice. Finally, our data support the notion of crosstalk between incretin biology and nAChR signaling, as we demonstrate that the glycemic benefits of glucagon-like peptide-1 receptor activation partially relies on beta4-containing nAChRs. Together, these data encourage further research into the role of cholinergic neurotransmission in regulating food reward and the translational pursuit of site-directed targeting of beta4-containing nAChRs for treatment of metabolic disease. |
