Newman B M, Lee P C, Tajiri H, Cooney D R, Lebenthal E
Am J Physiol. 1986 Jan;250(1 Pt 1):G103-8. doi: 10.1152/ajpgi.1986.250.1.G103.
Chronic pancreaticobiliary diversion was employed to study the modulation of enterokinase in the small intestine of adult rats. Diversion resulted in apparent trophic changes of the proximal bypassed portion of the intestinal mucosa. An almost complete loss of mucosal enterokinase activity in the proximal duodenum but no increase of enterokinase in the segments distal to reentry of the common duct was found in the pancreaticobiliary-diverted rats. The effect on the enterokinase activity in the proximal segment was specific in that no other brush-border enzymes measured in that segment were decreased. The decrease in enterokinase was partially prevented by dietary supplementation with pancreatic trypsinogen and completely avoided with the addition of a combination of bile acids and trypsinogen. Supplementation with bile acid alone did not preserve the enterokinase levels in the bypassed rats. The results suggested that trypsinogen is the primary factor responsible for modulating enterokinase levels in the proximal small intestine, with bile acids acting as a modifier.
采用慢性胰胆管转流术研究成年大鼠小肠中肠激酶的调节。转流导致肠黏膜近端旁路部分出现明显的营养变化。在胰胆管转流的大鼠中,发现十二指肠近端黏膜肠激酶活性几乎完全丧失,但在胆总管再进入远端的肠段中肠激酶没有增加。对近端肠段肠激酶活性的影响具有特异性,因为在该肠段中测量的其他刷状缘酶没有减少。通过饮食补充胰蛋白酶原可部分防止肠激酶减少,而添加胆汁酸和胰蛋白酶原的组合可完全避免这种情况。单独补充胆汁酸并不能维持旁路大鼠的肠激酶水平。结果表明,胰蛋白酶原是调节近端小肠肠激酶水平的主要因素,胆汁酸起修饰作用。