Objective: To determine the stability of individual differences in non-nutritive 'junk' palatable food (PF) intake in rats; assess the relationship of these differences to binge-eating characteristics and susceptibility to obesity; and evaluate the practicality of using these differences to model binge-eating and obesity. Design: Binge-eating prone (BEP) and resistant (BER) groups were identified. Differential responses to stress, hunger, macronutrient-varied PFs, a diet-induced obesity (DIO) regimen and daily vs intermittent access to a PF þ chow diet, were assessed. Subjects: One hundred and twenty female Sprague-Dawley rats. Measurements: Reliability of intake patterns within rats; food intake and body weight after various challenges over acute (1, 2, 4 h), 24-h and 2-week periods. Results: Although BEP and BER rats did not differ in amount of chow consumed, BEPs consumed 450% more intermittent PF than BERs (Po0.001) and consistently so (a ¼ 0.86). BEPs suppressed chow but not PF intake when stressed, and ate as much when sated as when hungry. Conversely, BERs were more affected by stress and ate less PF, not chow, when stressed and were normally hyperphagic to energy deficit. BEP overeating generalized to other PFs varying in sucrose, fat and nutrition content. Half the rats in each group proved to be obesity prone after a no-choice high fat diet (DIO diet) but a continuous diet of PF þ chow normalized the BEPs high drive for PF. Conclusion: Greater intermittent intake of PF predicts binge-eating independent of susceptibility to weight gain. Daily fat consumption in a nutritious source (DIO-diet; analogous to a fatty meal) promoted overeating and weight gain but limiting fat to daily non-nutritive food (PF þ chow; analogous to a snack with a low fat meal), did not. The data offer an animal model of lean and obese binge-eating, and obesity with and without binge-eating that can be used to identify the unique physiology of these groups and henceforth suggest more specifically targeted treatments for binge-eating and obesity.

Clinical binge eating runs a protracted course. The etiology of binge eating remains perplexing in part because, in humans, it is difficult to isolate and assess the independent and aggregate impact of various contributing variables. Using rats, we found that footshock stress and a history of caloric restriction (S+R), combine synergistically to induce binge eating. Stress and dieting are also strong antecedents and relapse factors in human eating disorders. Here we report further behavioral and physiological parallels to human binge eating. Like the protracted course of human binge eating, young female Sprague-Dawley rats continued to binge eat after 23 restriction/stress cycles (7 months) and this despite experiencing no significant weight loss during the restriction phases. Stress alone reduced adiposity by 35% (p<0.001) but S+R rats had no significant fat loss. An endocrine profile of normal plasma leptin and insulin levels but marked elevation of plasma corticosterone levels was found only in the binge-eating (S+R) rats (p<0.01), also paralleling endocrine profiles reported in clinical binge-eating studies. These behavioral and physiological similarities between this animal model and clinical binge eating increase its utility in understanding binge eating. Importantly, our findings also highlight the stubborn nature of binge eating: once a critical experience with dieting and stress is experienced, little if any further weight loss or food restriction is necessary to sustain it.

A history of dieting is common in individuals suffering from eating disorders for which depression and mood disturbances are also comorbid. We investigated the effect of a history of caloric restriction (HCR) in rats that involved cyclic food restriction and refeeding with varying levels of access to palatable food (PF) on: 1) responses to the SSRI, fluoxetine; 2) monoamine levels in brain regions central to the control of feeding, reward, and mood regulation; and 3) behavioral tests of anxiety and depression. HCR coupled with intermittent but not daily access to PF exaggerated rats' anorectic response to fluoxetine (p<0.05); was associated with a significant 71% and 58% reduction of 5-HT and dopamine, respectively, in the medial prefrontal cortex; and induced behaviors consistent with models of depression. HCR, irrespective of access to PF, abolished the strong association between 5-HT and dopamine turnover in the nucleus accumbens in control rats (r =0.71 vs. -0.06, p<0.01). Access to PF, irrespective of HCR, reduced hypothalamic dopamine. Together, these findings suggest that a history of frequent food restriction-induced weight fluctuation imposes neurochemical changes that negatively impact feeding and mood regulation.