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大鼠粪便中β-葡萄糖醛酸酶活性的胰胆和胆汁调控

Pancreatobiliary and biliary control of fecal beta-glucuronidase activity in the rat.

作者信息

Head M R, Fukumoto H E, Chang G W

机构信息

Department of Nutritional Sciences, University of California, Berkeley 94720.

出版信息

Cancer Lett. 1988 Apr;39(3):339-44. doi: 10.1016/0304-3835(88)90078-x.

Abstract

Bile duct ligation experiments suggest that bile is an important regulator of intestinal beta-glucuronidase, an enzyme thought to be involved in colon carcinogenesis. Exclusion of pancreatobiliary secretions from the rat intestine significantly decreases glucuronidase activity (Roberton et al., Cancer Res., 42 (1982) 5165-5166). However, the separate roles of pancreatic and biliary secretions have not been examined. We ligated the bile ducts of rats at the hepatic duct, allowing pancreatic juice but not bile to enter the intestine, or at the Sphincter of Oddi, excluding pancreatic juice as well as bile. Fecal beta-glucuronidase activity was lowered in both cases, indicating that bile itself, and not pancreatic juice, is a major factor modulating beta-glucuronidase activity.

摘要

胆管结扎实验表明,胆汁是肠道β-葡萄糖醛酸酶的重要调节因子,该酶被认为与结肠癌发生有关。排除大鼠肠道中的胰胆分泌物可显著降低葡萄糖醛酸酶活性(罗伯顿等人,《癌症研究》,42(1982)5165 - 5166)。然而,胰液和胆汁分泌的单独作用尚未得到研究。我们在肝管处结扎大鼠胆管,使胰液而非胆汁进入肠道,或在Oddi括约肌处结扎,排除胰液和胆汁。在这两种情况下,粪便中β-葡萄糖醛酸酶活性均降低,表明胆汁本身而非胰液是调节β-葡萄糖醛酸酶活性的主要因素。

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