• dieting;
  • binge eating disorder;
  • bulimia;
  • rats;
  • palatability



Dieting and stress are etiological factors in eating disorders, and dieting strongly predicts stress-induced overeating in the nonclinical population. We developed an animal model of binge eating in sated rats that is evoked by stress, but only in rats with a history of caloric restriction and only if highly palatable food (HPF) is available after stress. This study investigated the effect of known binge triggers, a taste of HPF and of hunger, on this type of binge eating.


Female rats were cycled through the R/S protocol but this time were given just a taste of HPF with ad lib regular chow. After another R/S cycle, rats were stressed during restriction (while hungry) and were given HPF and chow.


Although binge eating did not occur if only chow was available after stress, just a taste of HPF sufficed to increase chow intake to more than 160% (p < 0.001) of rats with a history of restriction only, stress-only, or neither. Hunger increased the proportion of chow consumed by both restricted groups, but stress magnified this hunger-induced overeating by increasing HPF intake to 137% of restriction-only rats (p < 0.001).


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. © 2003 by Wiley Periodicals, Inc. Int J Eat Disord 34: 183–197, 2003.