Estrogens inhibit food intake in CCK-1 receptor-deficient rats.

In human and many other animals, estrogens inhibit food intake and increases spontaneous activity. Previous studies hypothesized that the anorexigenic effect of estrogens is mediated by the cholecystokinin (CCK)-induced satiety effect. In the present study, we investigated whether estrogens-induced anorexigenic and hyper-active effects are present in Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rat, which is deficient in the CCK1 receptor. In OLETF rats with a regular 4-day estrous cycle, food intake decreased and spontaneous activity increased significantly more during estrus than diestrus as compared to control Long-Evans-Tokushima-Otsuka (LETO) rats. Subcutaneous injection of estradiol benzoate into ovariectomized OLETF rats significantly decreased feeding and increased spontaneous activity to the same extent as in LETO rats. These results suggest that the anorexigenic and hyper-active effects of estrogen can be mediated via pathways other than CCK-CCK1 receptor signaling pathway in CCK1 receptor-deficient rats.