Different Effects of Trypsin Inhibitors on Intestinal Gene Expression of Secretin and on Pancreatic Bicarbonate Secretion in CCK-A-Receptor-Deficient Rats

The Japanese Journal of Pharmacology

Shigenori Watanabe¹  Takao Shimazoe¹  Shinji Suzuki²  Akihiro Funakoshi³  Yutaka Takata³  Kyoko Miyasaka²  Setsuko Kanai²  Yuki Yoshida²  Takako Kawanami² 

[1] Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University;Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology;Department of Gastroenterology, National Kyushu Cancer Center

关键词: Cholecystokinin (CCK);    CCK-A receptor;    Bicarbonate;    Trypsin inhibitor;    Pancreas;   

DOI  :  10.1254/jjp.81.339

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(32)Cited-By(5)The effects of oral administration of two synthetic trypsin inhibitors (camostate and ONO-3403) and soybean trypsin inhibitor (SBTI) on cholecystokinin (CCK), secretin gene expression and pancreatic secretion were examined in CCK-A-receptor-deficient (OLETF) rats. The rats were fed chow containing 0.1% trypsin inhibitors for 7 days. To examine pancreatic secretion, the rats were prepared with cannulae to drain the bile and pancreatic juice separately, a duodenal cannula and an external jugular vein cannula. The animals were maintained in Bollman cages and the experiments were conducted 4 days after surgery. The levels of CCK mRNA were significantly increased by each treatment. The levels of secretin mRNA were significantly increased by camostate and SBTI, but not by ONO-3403. Bicarbonate secretion was significantly increased in rats treated with camostate and ONO-3403, but not SBTI, while protein secretion was not affected by any treatment. These observations suggest that increased bicarbonate secretion produced by synthetic trypsin inhibitors in CCK-A-receptor-deficient rats may not be due to secretin but due to ONO-3403 in the circulation.

【 授权许可】

Unknown