Influence of the ovarian cycle and estradiol in frustration stress-induced binge-like palatable food consumption in female rats with a history of food restriction

Eating disorders show marked gender differences [1] and several epidemiologic studies suggest that binge eating episodes are more common in females than in males [2]. To further investigate the mechanisms underlying this sex difference, we used an animal model first described by Cifani et al. [3], in which binge eating is evoked in female rats by food restriction followed by frustration stress (15 min exposure to the sight of the palatable food). We aimed to determine whether binge eating behavior varies across the estrus cycle and is influenced by estradiol in ovariectomized (OVX) rats. Finally, using immunocytochemistry, we quantified the activation of extracellular signal regulated kinase (ERK) signaling pathway in OVX rats treated with estradiol or oil vehicle, in basolateral (BLA) and the central (CeA) nuclei of the amygdala, paraventricular nucleus of hypothalamus (PVN) and arcuate nucleus (ARC). Restricted and stressed non-estrus rats showed binge eating behavior in comparison to the control not restricted and not stressed rats. This response was not present in restricted and stressed rats in estrus, and in OVX rats treated with estradiol. This lack of binge eating behavior was accompanied by a significant decrease in ERK phosphorylation in ARC, PVN and in the CeA, but not in BLA, in comparison to non-estrous rats and to not restricted and not stressed animals. Our behavioral findings show that binge eating does not occur during the estrous phase. Because this was recapitulated in OVX rats treated with estradiol, we propose that the inhibitory effect of estradiol on eating is partly responsible for the lack of bingeing. These findings are consistent with reports in women with bulimia nervosa [4], in whom the binge frequency decreased during the follicular phase, a time of the menstrual cycle when eating is also lowest. These results extend our previous findings and increase the validity of our model, such that it can be used in translational studies of the mechanism of binge eating behavior. References: [1] Klump et al. 2008 Psych Med 38:1749-57 [2] Cifani et al. 2009 Psychopharmology 204:113-125 [3] Hudson et al. 2007 Biol Psychiatry 61:348-358 [4] Edler et al. 2007 Psych Med 37:131-141