cholecystokinin-39 and osteum

To describe the secretory responses to physiological stimulation of the exocrine pancreas after partial pancreatectomy in conscious animals.. Controlled study.. Thirteen mongrel dogs.. Partial pancreatectomy (n = 4), and creation of gastric and pancreatic (Herrera) fistulas (n = 13). Collections of duodenal juice at 15 minute intervals after an oral meal or during intraduodenal infusion of sodium oleate, and blood samples.. Protein concentration in duodenal juice and cholecystokinin 33/39 concentrations in plasma one and three months after partial pancreatectomy, and secretion of fluid by the pancreas.. Pancreatic protein output after a meal was significantly reduced at one and three months in dogs after partial pancreatectomy compared with control animals. Protein output in response to an intraduodenal infusion of oleate was also reduced at both time points. In contrast, secretion of fluid after a meal or during infusion of oleate was unchanged by removal of the distal lobe. There was no correlation between the effects of partial pancreatectomy on protein output and plasma concentrations of cholecystokinin 33/39.. Pancreatic exocrine deficiency, particularly the reduction in secretion of protein, results directly from the partial pancreatectomy and persists for at least three months after the operation.

Topics: Animals; Cholecystokinin; Dogs; Eating; Exocrine Pancreatic Insufficiency; Oleic Acid; Oleic Acids; Pancreatectomy; Pancreatic Juice; Proteins

Amylase secretion and plasma cholecystokinin (CCK) were measured in dogs in the interdigestive state and after exogenous CCK-8 and CCK-39 (12.5 to 400 pmol.kg-1.h-1), intestinal sodium oleate, tryptophan plus phenylalanine, HCl (0.74, 2.2, 6.7, 20 mmol/h), and a meat meal (20 g/kg). Interdigestive plasma CCK did not vary, although amylase output showed periodic 15-fold increases. Plasma CCK increased linearly after doubling doses of CCK-8 and CCK-39; the slope of plasma CCK-39 vs. dose was 2.8 times steeper than that of CCK-8, suggesting a longer circulating half-life. At similar plasma concentrations, CCK-8 and CCK-39 were equipotent for stimulating pancreatic secretion. Sodium oleate and tryptophan plus phenylalanine significantly increased plasma CCK and amylase secretion in a load-dependent pattern and were equipotent for both effects. HCl stimulated bicarbonate secretion but not plasma CCK or amylase secretion. Food significantly increased plasma CCK and amylase secretion. Amylase responses to intestinal stimulants and food were significantly greater than to exogenous CCK at low plasma CCK levels. Maximal amylase responses to intestinal stimulants were similar to that after CCK-39 but occurred at 10-fold lower plasma CCK levels. These results indicate that CCK and other factors interact to regulate pancreatic responses to food and intestinal stimulants in dogs.

Topics: Amylases; Animals; Cholecystokinin; Dogs; Eating; Injections, Intravenous; Intestines; Oleic Acid; Oleic Acids; Pancreas; Phenylalanine; Sincalide; Tryptophan

Peptide YY inhibits the pancreatic exocrine secretion (bicarbonate, water, and protein) that is stimulated by cholecystokinin, secretin, or neurotensin in the dog, but whether peptide YY inhibits the release of gut peptides that stimulate pancreatic exocrine secretion is not known. Six dogs were prepared with gastric, pancreatic, and cecal cannulas. On separate days, a single dose of sodium oleate (3, 6, 7.5, 9, 12, 15, or 18 mmol/h) was given intraduodenally for 90 min, either alone (control) or in combination with peptide YY (25, 50, 100, 200, or 400 pmol/kg.h, i.v.). We measured plasma levels of cholecystokinin-33/39, secretin, neurotensin, and peptide YY by radioimmunoassay. During infusion of peptide YY, the integrated release of cholecystokinin (3.3 +/- 0.5 ng-[0-90] min/ml) was decreased significantly (p less than 0.05) when compared with control values (5.6 +/- 0.6). Release of secretin and neurotensin was not affected. A positive correlation (p less than 0.05) was found between the release of cholecystokinin and pancreatic protein output in both control (r = 0.68) and peptide YY-treated (r = 0.67) groups. Release of peptide YY was significant after intraduodenal or intracolonic administration of sodium oleate. These studies demonstrate that inhibition of pancreatic protein secretion by peptide YY in dogs is mediated, at least in part, by an inhibition of the release of cholecystokinin.

Topics: Animals; Cholecystokinin; Dogs; Female; Gastrointestinal Hormones; Male; Neurotensin; Oleic Acid; Oleic Acids; Pancreas; Peptide Fragments; Peptide YY; Peptides; Secretin