The role of alpha-7 nicotinic receptors in food intake behaviors

Abstract

Nicotine alters appetite and energy expenditure, leading to changes in body weight. While the exact mechanisms underlying these effects are not fully established, both central and peripheral involvement of the alpha-7 nicotinic acetylcholine receptor (alpha7nAChR) has been suggested. Centrally, the alpha7nAChR modulates activity of hypothalamic neurons involved in food intake regulation, including proopiomelanocortin and neuropeptide Y. alpha7nAChRs also modulate glutamatergic and dopaminergic systems controlling reward processes that affect food intake. Additionally, alpha7nAChRs are important peripheral mediators of chronic inflammation, a key contributor to health problems in obesity. This review focuses on nicotinic cholinergic effects on eating behaviors, specifically those involving the alpha7nAChR, with the hypothesis that alpha7nAChR agonism leads to appetite suppression. Recent studies are highlighted that identify links between alpha7nAChR expression and obesity, insulin resistance, and diabetes and describe early findings showing an alpha7nAChR agonist to be associated with reduced weight gain in a mouse model of diabetes. Given these effects, the alpha7nAChR may be a useful therapeutic target for strategies to treat and manage obesity.