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To clarify a physiological role of endogenous peptide YY(PYY) on pancreatic exocrine secretion, gastrointestinal transit and bile flow, a hyper-PYY-emia model was constructed by performing a massive small bowel resection using rats. (1) 75% resection of the small intestine was performed at its distal side. Two weeks after surgery, these rats were fed a liquid meal, and intestinal transit of contents was observed and plasma PYY and secretin concentrations were measured by radioimmunoassay. (2) Two weeks after the same surgery, a liquid meal was infused into the duodenum, and both pancreatic juice and bile were collected separately under general anesthesia. Transit of the intestinal contents from the pyloric ring, plasma CCK concentrations, pancreatic juice flow, amylase output, and bile flow were determined. Hyper-PYY-emia occurred following surgery both at fasting and after feeding, accompanied by retardation of gastrointestinal transit, increase of pancreatic juice flow and decrease of bile flow. Plasma secretin levels were elevated slightly, while CCK levels remained unchanged. In conclusion, massive small bowel resection is a useful model to induce hyper-PYY-emia in rats. It is considered that, in a malnutritional state after small intestinal resection, a colonic regulatory mechanism, via humoral factors such as PYY, participates in the feedback regulation of proximal intestinal as well as of pancreatic function.

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We experienced a case of minute pancreatic carcinoma in a 59-year-old man who complained of upper abdominal pain after drinking alcohol. Abdominal ultrasonography (US) revealed dilatation of the main pancreatic duct (MPD). Abdominal computed tomography (CT) and magnetic resonance cholangiopancreatography (MRCP) showed slight dilatation of the MPD and its obstruction near the portal vein. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated occlusion of the MPD, and cytology of aspirated pancreatic juice was negative for malignancy. With the diagnosis of benign localized obstruction of the MPD, the patient underwent surgery. There was a clear demarcation of hardness and color of the pancreas on the left margin of the superior mesenteric vein, and the caudal pancreas was hard and fibrotic. Intraoperative US revealed slight dilatation of the MPD, and the aspiration cytology result was class IV. First, segmental resection of the pancreas was performed, but pathological examination of frozen section showed neither malignancy nor stenotic lesion. An additional small portion of the proximal pancreas was resected. The specimen included a ductal carcinoma, 5 mm in diameter. Accordingly, a pylorus-preserving pancreatoduodenectomy was performed. Microscopically, the minute carcinoma had already penetrated the duct wall and infiltrated lymph vessels and veins. The patient has been under close observation at our outpatient clinic, and so far there have been no signs of recurrence. To improve the poor prognosis of pancreatic cancer, we should be alert to the occurrence of acute pancreatitis as an initial symptom.

The pathophysiology following a total colectomy with ileal pouch-anal anastomosis (IPAA) has not been sufficiently clarified yet. We investigated bile acid metabolism, bacterial bowel flora and transit of the alimentary tract after IPAA, with reference to administration of ursodeoxycholic acid (UDCA) in dogs undergoing IPAA. Ten adult beagle dogs underwent IPAA at one stage, and were observed for 12 months. UDCA (100 mg/day) was administered orally to five dogs, and the other five did not. In the UDCA(+) group, UDCA replaced other bile acids, especially cholic acid, accounting for 16.5% of gallbladder bile at 12 months after surgery. Both plasma levels and postprandial increase of total bile acids remained unchanged in the UDCA(+) group, but decreased in the UDCA(-) group at 12 months. Fecal excretion of bile acids tended to be smaller in the UDCA(+) group, and the ratio of secondary to primary bile acids was larger in the UDCA(-) group. Almost all the bile acids were in free form in stool, and UDCA constituted 19% in the UDCA(+) group. The transit time of the whole alimentary tract was elongated by administering UDCA, especially at an early period after IPAA. Although both anaerobic and aerobic bacteria decreased after IPAA, the latter decreased more in stool, resulting in an increase in the ratio of total anaerobes/total aerobes, especially in the UDCA(-) group. The decrease in Bacteroidaceae and Lactobacillus after IPAA was slightly smaller in the UDCA(+) group. Administration of UDCA following IPAA was efficient to induce rapid intestinal adaptation and also to keep the bile acid fraction in the ileal pouch less harmful.

Dogs with a vagally denervated (Heidenhain) pouch and a gastric fistula were used to investigate the humoral mechanism which would affect the gastric acid secretion following acute intragastric ethanol administration. Ethanol solutions induced a doserelated secretion of gastric acid. Although plasma gastrin levels increased after the loading of both 20% and 30% ethanol solutions, there was a discrepancy between total acid output and the integrated gastrin response. Plasma secretin levels also augmented after the administration of ethanol solutions, with a delay of about one hour after the onset of acid secretion. The response of gastric inhibitory polypeptide (GIP) to ethanol was very slight, similar to that of insulin. There was a significant rise in plasma glucose levels after the instillation of 30% ethanol solution as in the case of liquid meal. It is concluded that gastrin may be merely one of the factors which stimulate acid secretion after ethanol administration, and that gastric acid would have a close relationship with secretin release. It is also probable that acid is not an effecitve stimulant to the release of GIP.intragastric ethanol administration ; gastric acid secretion ; gastrin ; secretin ; GIP Since 1898 (Chittenden et al. ), many investigators have reported the relationship between alcohol intake and gastric acid secretion. However, their results did not always agree. Some persons showed the stimulatory effect of alcohol on gastric acid secretion (Hirschowitz et al. 1956;Woodward et al. 1957;Lenz et al. 1983), others reported the opposite (Cooke 1972;Kuo and Shanbour 1983). Regarding the mechanism by which alcohol affects acid secretion, many factors (such as species differences, route of administration, etc.) have been pointed out by those researchers. Moreover, as remarkable advances in the study of gastrointestinal hormones have been made, some hormones (e.g. gastrin and secretin) have been referred to as substances which mediate the action of alcohol on gastric acid

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