Moran T H
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Nutrition. 2000 Oct;16(10):858-65. doi: 10.1016/s0899-9007(00)00419-6.
In the almost 30 years since the ability of peripheral administration of the brain/gut peptide cholecystokinin (CCK) to inhibit food intake was first demonstrated, significant progress in our overall understanding of the role of CCK in ingestive behavior has been made. A physiologic role for endogenous CCK in the control of meal size has been demonstrated and sites and mechanisms of action for CCK in food intake have been investigated. Recent work has uncovered roles for the CCK satiety pathway in the mediation of the feeding modulatory actions of estradiol, insulin, and leptin. The availability of the Otsuka Long Evans Tokushima Fatty (OLETF) rat, a strain lacking CCK(A) receptors, provides a unique model for the study of how deficits in a within-meals satiety signaling pathway may result in long-term changes in food intake and body weight.
自首次证明经外周给予脑/肠肽胆囊收缩素（CCK）具有抑制食物摄入的能力以来，在近30年的时间里，我们对CCK在摄食行为中作用的总体认识取得了重大进展。内源性CCK在控制进餐量方面的生理作用已得到证实，并且对CCK在食物摄入中的作用位点和作用机制进行了研究。最近的研究发现，CCK饱腹感途径在介导雌二醇、胰岛素和瘦素的进食调节作用中发挥作用。大冢长-伊-德岛肥胖（OLETF）大鼠是一种缺乏CCK（A）受体的品系，它为研究餐内饱腹感信号通路缺陷如何导致食物摄入量和体重的长期变化提供了一个独特的模型。
