雌激素可抑制 CCK-1 受体缺陷型大鼠的摄食。
Estrogens inhibit food intake in CCK-1 receptor-deficient rats.
机构信息
Department of Integrative Physiology, Faculty of Medical Sciences, University of Fukui, Eiheiji-cho, Matsuoka, Fukui, 910-1193, Japan.
出版信息
J Physiol Sci. 2010 Jul;60(4):267-71. doi: 10.1007/s12576-010-0094-y. Epub 2010 May 22.
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.
在人类和许多其他动物中，雌激素抑制食物摄入并增加自发活动。先前的研究假设雌激素的厌食作用是通过胆囊收缩素（CCK）诱导的饱腹感作用介导的。在本研究中，我们研究了缺乏 CCK1 受体的 Otsuka-Long-Evans-Tokushima-Fatty（OLETF）大鼠是否存在雌激素诱导的厌食和多动效应。在具有正常 4 天发情周期的 OLETF 大鼠中，与对照 Long-Evans-Tokushima-Otsuka（LETO）大鼠相比，发情期的食物摄入量明显减少，自发活动明显增加。将苯甲酸雌二醇皮下注射到去卵巢的 OLETF 大鼠中，可显著减少摄食并增加自发活动，其程度与 LETO 大鼠相同。这些结果表明，在缺乏 CCK1 受体的大鼠中，雌激素的厌食和多动作用可以通过 CCK-CCK1 受体信号通路以外的途径介导。
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