Strubbe J H, Wolsink J G, Schutte A M, Balkan B, Prins A J
Department of Animal Physiology, University of Groningen, Haren, The Netherlands.
Physiol Behav. 1989 Oct;46(4):643-6. doi: 10.1016/0031-9384(89)90345-4.
In order to compare effects of circulating CCK-8 and glucagon on food intake, rats were provided with a permanently implanted catheter in the right atrium. Another cannula was implanted into the hepatic-portal vein by a new technique. After a standard fasting period graded loads of CCK-8 and glucagon were infused via these catheters during refeeding. Intracardiac glucagon and CCK loads dose-dependently suppressed meal size. Intraportal infusion of glucagon caused similar suppression compared to intracardiac administration. This may indicate a minor role of the liver as a target for the suppression of feeding by glucagon. In contrast, intraportal infusion of CCK-8 did not reduce food intake. The results indicate that CCK-8 is removed or inactivated by the liver. It is suggested that CCK-8 acts locally on vagal nerve endings to exert its suppressive action on food intake.
为了比较循环中的胆囊收缩素-8（CCK-8）和胰高血糖素对食物摄入量的影响，给大鼠的右心房永久性植入一根导管。通过一种新技术将另一根套管植入肝门静脉。在标准禁食期后，在重新喂食期间通过这些导管注入不同剂量的CCK-8和胰高血糖素。心内注射胰高血糖素和CCK的剂量依赖性地抑制进食量。与心内给药相比，门静脉内注射胰高血糖素引起类似的抑制作用。这可能表明肝脏作为胰高血糖素抑制进食的靶点作用较小。相反，门静脉内注射CCK-8并没有减少食物摄入量。结果表明CCK-8被肝脏清除或失活。提示CCK-8在迷走神经末梢局部起作用，对食物摄入发挥抑制作用。
