peptide-yy and osteum

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

In the present study we report methods for the isolation and culture of colonic peptide YY (PYY) cells and have tested the effects of sodium oleate and other chemotransmitters on PYY release. Enzyme-dispersed canine colonic mucosa cells were separated by a Beckman elutriation rotor, and the enriched PYY fraction was cultured on type I collagen in full growth medium. After 42-48 h of culture PYY cells had selectively adhered to the collagen. Forty to 45% of the adherent cells contained PYY (5.5 +/- 0.5 pmol/24-mm well), and 10-15% of the cells contained glucagon-like immunoactivity (GL29-LI; 0.95 pmol/24-mm well). The effect of various secretagogues on PYY release from these cultures was monitored. Sodium oleate stimulated PYY release in a time-dependent fashion over a dose range from 10 microM to 10 mM. However, sodium oleate at a dose of 100 mM produced disproportionately large PYY release. During a 2-h incubation 5.1% of the total cell content of PYY was released in response to 0.1 mM sodium oleate compared with basal release of 1.1%. At doses less than 10 mM sodium oleate did not release GL29-LI, whereas concentrations of 10 and 100 mM resulted in marked GL29-LI release. These findings suggest that lower concentrations of sodium oleate selectively release PYY, whereas higher concentrations nonselectively induce peptide release probably by effects on membrane stability. We also found that bombesin, epinephrine, and forskolin, but not carbachol, produced time- and dose-dependent release of PYY from these cultures.

Topics: Animals; Bombesin; Cells, Cultured; Colon; Dogs; Dose-Response Relationship, Drug; Gastrointestinal Hormones; Glucagon-Like Peptides; Immunohistochemistry; Microscopy, Electron; Oleic Acid; Oleic Acids; Peptide YY; Peptides; Radioimmunoassay