Wisner J R, Ozawa S, Xue B G, Renner I G
Pancreatico-Biliary Research Institute, Hospital of the Good Samaritan, Los Angeles, CA 90017.
Pancreas. 1990 Jul;5(4):434-8. doi: 10.1097/00006676-199007000-00010.
We examined whether endogenous cholecystokinin (CCK) is involved in growth of the preweanling rat pancreas. Twice daily for 14 days, 7-day-old neonatal rats received an oral gavage of either 2.5 mg/kg or 5.0 mg/kg of the potent and specific CCK receptor antagonist L-364,718 (the 2.5 mg/kg dose of antagonist was shown in the present study to abolish totally the pancreas growth-promoting effects of exogenously administered caerulein (CR) in neonatal rats). Control pups received oral gavages of the L-364,718 vehicle alone. The final body weights, pancreas weights, total pancreatic DNA contents, and total pancreatic protein contents did not differ significantly between the 21-day-old control pups and the 21-day-old pups that were pretreated for 14 days with either the low or the high doses of L-364,718. These findings suggest that endogenous CCK is not required for growth of the neonatal rat pancreas.
我们研究了内源性胆囊收缩素（CCK）是否参与幼龄大鼠胰腺的生长。7日龄新生大鼠每天接受两次口服灌胃，持续14天，灌胃剂量分别为2.5mg/kg或5.0mg/kg的强效特异性CCK受体拮抗剂L-364,718（本研究表明，2.5mg/kg剂量的拮抗剂可完全消除外源性蛙皮素（CR）对新生大鼠胰腺生长的促进作用）。对照幼崽仅接受L-364,718赋形剂的口服灌胃。21日龄对照幼崽与用低剂量或高剂量L-364,718预处理14天的21日龄幼崽之间，最终体重、胰腺重量、胰腺总DNA含量和胰腺总蛋白含量均无显著差异。这些发现表明，内源性CCK并非新生大鼠胰腺生长所必需。
