Takako Kawanami1,2, Shinji Suzuki1, Yuki Yoshida1,
Setsuko Kanai1, Yutaka Takata2,
Takao Shimazoe3, Shigenori Watanabe3, Akihiro Funakoshi2 and Kyoko Miyasaka1,*
1Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173 - 0015, Japan
2Department of Gastroenterology, National Kyushu Cancer Center, Fukuoka 811 - 1395, Japan
3Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka 812 - 8582, Japan
* To whom correspondence should be addressed.
Abstract: 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.
Keywords: Cholecystokinin (CCK), CCK-A receptor, Bicarbonate, Trypsin inhibitor, Pancreas