Departments of Psychology and of Medicine, The Diabetes Research Center, and The Regional Primate Research Center, University of Washington, USA.
The Seattle Veterans Administration Hospital, Seattle, Washington, USA.
Diabetologia. 1981 Mar;20(Suppl 1):305-313. doi: 10.1007/BF00254497.
There are now a large number of experiments demonstrating that peripheral administration of exogenous cholecystokinin or its synthetic analogue, CCK-8, reduces meal size in a number of species. The peptide interacts with other factors which influence satiety, and treatments thought to be effective in eliciting secretion of cholecystokinin have predictable effects on meal size. Cholecystokinin is effective in the genetically obese Zucker rat, obese rats with lesions of the ventromedial hypothalamus, and subdiaphragmatically vagotomized rats. Somatostatin and bombesin are also reasonable candidates for satiety factors. Intraperitoneal naloxone reduces meal size in rats, and beta-endorphin injected intraventricularly causes an increase in meal size of 50% over 30 minutes. We conclude that cholecystokinin and bombesin may interact in weight regulation and control of meal time food intake.
现在有大量实验证明,外源性胆囊收缩素或其合成类似物 CCK-8 可减少多种物种的进食量。该肽与影响饱腹感的其他因素相互作用,并且被认为可有效引发胆囊收缩素分泌的治疗方法对进食量具有可预测的影响。胆囊收缩素在遗传性肥胖 Zucker 大鼠、腹内侧下丘脑损伤的肥胖大鼠和膈下迷走神经切断大鼠中均有效。生长抑素和 bombesin 也是饱腹感因素的合理候选者。腹腔内给予纳洛酮可减少大鼠的进食量,脑室注射β-内啡肽可使 30 分钟内的进食量增加 50%。我们得出结论,胆囊收缩素和 bombesin 可能在体重调节和控制进食时间的食物摄入方面相互作用。