Combined dieting and stress evoke exaggerated responses to opioids in binge-eating rats.

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.

Stress and hunger alter the anorectic efficacy of fluoxetine in binge-eating rats with a history of caloric restriction.

Objective: We examined the effect of fluoxetine to suppress binge eating in rats with a history of caloric restriction (CR) and the extent to which this effect was altered by stress and hunger.

Method: To detect heightened sensitivity to fluoxetine, young female rats were used to determine a subthreshold anorectic dose (2 mg/kg, intraperitonally). Another group of rats was either fed ad libitum or given multiple CR (to 90% body weight) and refeeding-to-satiety cycles.

The role of palatable food and hunger as trigger factors in an animal model of stress induced binge eating.

Objective: 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.