Postponement of satiety by blockade of brain cholecystokinin (CCK-B) receptors.
Postponement of satiety by blockade of brain cholecystokinin (CCK-B) receptors.
复制标题
通过阻断脑胆囊收缩素 (CCK-B) 受体来推迟饱腹感。
作者：
C. Dourish;W. Rycroft;S. Iversen
外源性胆囊收缩素（cholecystokinin，CCK）可减少动物和人的摄食量并引起饱腹感，但内源性CCK引起饱腹感以及这种反应是否由外周型（CCK-A）或脑型（CCK-B）受体介导尚不清楚。CCK-A（MK-329）和CCK-B（L-365，260）受体的强效和选择性拮抗剂的开发现在可以解决这些问题。CCK-A拮抗剂MK-329和CCK-B拮抗剂L-365，260可增加部分饱食大鼠的摄食量，并推迟饱食感的发生;然而，L-365，260在增加摄食和预防饱食感方面的效力比MK-329强100倍。这些结果表明，内源性CCK通过对脑中CCK-B受体的激动剂作用引起饱腹感。
Exogenous cholecystokinin (CCK) decreases food intake and causes satiety in animals and man. However, it has not been established that endogenous CCK causes satiety or whether the response is mediated by peripheral-type (CCK-A) or brain-type (CCK-B) receptors. The development of potent and selective antagonists for CCK-A (MK-329) and CCK-B (L-365,260) receptors now allows these issues to be addressed. The CCK-A antagonist MK-329 and the CCK-B antagonist L-365,260 increased food intake in partially satiated rats and postponed the onset of satiety; however, L-365,260 was 100 times more potent than MK-329 in increasing feeding and preventing satiety. These results suggest that endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain.