These effects suggest that binge eating in this model is motivated by reward, not metabolic need, and parallels observations of binge triggers described in clinical binge-eating disorders. This strengthens the validity of using this animal model to target the physiology and treatment of eating disorders preceded by dieting and stress.

The authors developed an animal model of binge eating where history of caloric restriction with footshock stress (R + S) causes rats to consume twice the normal amount of palatable food. The authors tested the hypothesis that binge eating is mediated by changes in opioid control of feeding by comparing rats' anorectic and orexigenic responses to naloxone and butorphanol, respectively, and by testing the ability of butorphanol to elicit binge eating of chow when palatable food was absent. Mu/kappa opioid-receptor blockade and activation had exaggerated responses in the R + S rats with naloxone suppressing binge eating to control levels, and although butorphanol did not trigger chow binge eating, it enhanced binge eating of palatable food. These responses in sated normal-weight rats strengthen evidence that reward, over metabolic need, drives binge eating.

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Results support the utility of this animal model to elucidate serotonergic changes linking dieting to binge eating. The diverse effects of fluoxetine on the type of food, and in hungry versus sated rats, suggest alternate brain mechanisms should be concomitantly targeted for improved treatment of binge eating disorders.