Smith G P, Gibbs J, Jerome C, Pi-Sunyer F X, Kissileff H R, Thornton J
Peptides. 1981;2 Suppl 2:57-9. doi: 10.1016/0196-9781(81)90011-5.
The satiety effect of cholecystokinin (CCK) that was first observed in rats has now been extended to chickens, rabbits, pigs, sheep, rhesus monkeys, lean mice, genetically obese mice and rats, neurologically obese rats, lean men and women, and obese men. The effect is specific and can be obtained in animals and humans without reports or signs of sickness. The mechanism of the effect is unknown, but the gastric vagal fibers are necessary for the effect. This has led to the hypothesis that the satiety effect is due to activation of vagal afferent fibers that inhibit the central control system of feeding by CCK acting directly on recently described vagal CCK receptors and/or indirectly through a gastric smooth muscle effect that vagal receptors are sensitive to.
最初在大鼠身上观察到的胆囊收缩素(CCK)的饱腹感效应,现已扩展到鸡、兔、猪、羊、恒河猴、瘦小鼠、遗传性肥胖小鼠和大鼠、神经学肥胖大鼠、瘦男性和女性以及肥胖男性。这种效应具有特异性,在动物和人类身上均可获得,且无疾病报告或症状。该效应的机制尚不清楚,但胃迷走神经纤维对该效应是必需的。这导致了一种假说,即饱腹感效应是由于迷走传入纤维的激活,CCK通过直接作用于最近描述的迷走CCK受体和/或间接通过迷走受体敏感的胃平滑肌效应来抑制进食的中枢控制系统。