Abstract
Binge eating disorder (BED) is characterized by dysfunctional hedonic food intake and reward-related processes. Activation of the serotonin (5-HT) 5-HT2C receptor (5-HT2CR) suppresses both food intake and reward-related behaviors and is thus poised to regulate BED. This study assessed the effects of 5-HT2CR activation via the selective 5-HT2CR agonist WAY163909 on binge eating-related behaviors in adult male Sprague-Dawley rats. Low doses of WAY163909 (1.0, 2.0 mg/kg) suppressed high-fat food (HFF) binge intake, but not standard food non-binge intake. WAY163909 (1.0 mg/kg) also attenuated operant responding for self-administered HFF pellets on fixed and progressive ratio schedules of reinforcement, indicating that 5-HT2CR activation suppresses the reinforcing and motivational properties of HFF, respectively. These findings suggest that activation of the 5-HT2CR may be effective at suppressing binge eating in patients with BED via suppression of the reinforcing and motivational properties of HFF. This work supports future studies targeting the 5-HT2CR in the treatment of BED.
Highlights
Binge eating disorder (BED) is characterized by uncontrollable, recurrent episodes of excessive intake of food (American Psychiatric Association, 2013)
Food intake can be described as homeostatic or hedonic
Hedonic processes are postulated as an important component of binge eating episodes seen in disorders such as BED (Finlayson et al, 2011)
Summary
Binge eating disorder (BED) is characterized by uncontrollable, recurrent episodes of excessive intake of food (American Psychiatric Association, 2013). Food intake during binge episodes is often driven by hedonic rather than homeostatic mechanisms (i.e., food intake driven by wanting and liking factors but not necessary for energy balance; Finlayson et al, 2011; Dalton et al, 2013; Witt and Lowe, 2014). Patients with BED deem high-fat foods (HFFs) more rewarding than people without BED, which may motivate them to consume palatable food (Schebendach et al, 2013), and exhibit disruptions in reward neurocircuitry (Kessler et al, 2016). One avenue to identify novel treatment approaches in BED is to explore targets known to alter both food intake and reward-related behaviors. The serotonin (5-HT) 5-HT2C receptor (5-HT2CR) fulfills these criteria in that previous studies have demonstrated that 5-HT2CR activation suppresses feeding behavior (Hewitt et al, 2002; Bickerdike, 2003; Voigt and Fink, 2015) via promotion of satiety
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