Kanayama S, Himeno S, Yamasaki Y, Shinomura Y, Kitani T, Tarui S
Gastroenterol Jpn. 1987 Apr;22(2):211-7. doi: 10.1007/BF02774219.
A sensitive and specific radioimmunoassay system for rat plasma cholecystokinin (CCK) was employed to study the effect of trypsin inhibitor on plasma CCK levels. Feeding the trypsin inhibitor, FOY-305 200 mg/kg, to rats for 10 days stimulated the pancreatic growth. However, there was no significant difference in fasting plasma concentrations and duodenal contents of CCK and secretin. On the other hand, acute ingestion of same dosage of FOY-305 caused a marked (20-fold) and sustained elevation of plasma CCK levels. The principal form of circulating CCK was CCK-22 like on Sephadex G-50, in contrast to that of the cerebrum and duodenum where CCK-8 like form, or CCK-8 and CCK-22 like forms were main components, respectively. A significant rise in plasma levels of immunoreactive secretin was also found. These results suggest that the pancreatic growth observed by feeding the trypsin inhibitor to rats is caused by an excessive amount of CCK in conjunction with secretin.
采用一种灵敏且特异的大鼠血浆胆囊收缩素（CCK）放射免疫分析系统，研究胰蛋白酶抑制剂对血浆CCK水平的影响。给大鼠喂食200mg/kg的胰蛋白酶抑制剂FOY - 305，持续10天，可刺激胰腺生长。然而，空腹血浆中CCK和促胰液素的浓度以及十二指肠内容物并无显著差异。另一方面，急性摄入相同剂量的FOY - 305会导致血浆CCK水平显著（20倍）且持续升高。在葡聚糖凝胶G - 50上，循环CCK的主要形式类似CCK - 22，这与大脑和十二指肠不同，在大脑中主要成分是类似CCK - 8的形式，在十二指肠中主要成分分别是类似CCK - 8和CCK - 22的形式。还发现免疫反应性促胰液素的血浆水平显著升高。这些结果表明，给大鼠喂食胰蛋白酶抑制剂所观察到的胰腺生长是由过量的CCK与促胰液素共同作用引起的。
