Body composition and endocrine status of long-term stress-induced binge-eating rats

Abstract

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.

Figure 1

Chow and palatable food (PF) intake over 0–4 hrs after onset of dark of control rats (Control), of rats following footshock stress (Stress), of rats after a history of caloric restriction-refeeding (Restrict), and rats with a history of caloric restriction-refeeding after stress (S+R) following 3 traditional initial “long” cycles (A); after 5 restriction-refeeding/stress cycles, the last 2 which were “short” cycles(B); after 12 restriction-refeeding/stress cycles, the last 9 which were “short” cycles (C), and after 23 restriction-refeeding/stress cycles, the last 20 being “short” cycles (D).

Figure 2

Post-sacrifice percent of body weight as fat after 23 cycles for Control rats that were never stressed or restriction-refeeding cycled, Stress rats that were only stressed, Restrict rats that were only restriction-refeeding cycled and the binge-eating S+R rats that were stressed and restriction-refeeding cycled; ***p<0.001 Stress vs. all other groups.

Figure 3

(A) Levels of plasma leptin in rats with stress and restriction-refeeding cycles (S+R; dark bar) compared to control rats (Control), rats with only stress (Stress), and rats with only a restriction-refeeding cycling (Restrict); * p<0.05 Stress vs. Control and Restrict only; ** p<0.01 main effect of stress to decrease leptin, an effect statistically accounted for by decreased body fat. (B) Plasma glucose levels for all groups; ns. (C) Plasma insulin levels for all groups; *p<0.05 main effect of stress, also statistically accounted for by decreased body fat in stressed groups. (D) Plasma glucose/insulin ratio for all groups; ns.

Figure 4

Level of plasma corticosterone in rats with stress and a history of restriction (S+R) compared to control rats (Control), rats with only stress (Stress), and rats with only a history of restriction (Restrict); ***p<0.001 S+R vs. all groups.