A physiological role of peptide YY on exocrine pancreatic secretion in rats

1993 ◽  
Vol 105 (1) ◽  
pp. 208-215 ◽  
Author(s):  
Haiou Jin ◽  
Lixing Cai ◽  
Kaeyol Lee ◽  
Ta-Ming Chang ◽  
Ping Li ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Peptide Yy ◽  
Physiological Role ◽  
Exocrine Pancreatic Secretion

An important role of endogenous insulin on exocrine pancreatic secretion in rats

1990 ◽  
Vol 258 (2) ◽  
pp. G268-G274 ◽  
Author(s):  
K. Y. Lee ◽  
L. Zhou ◽  
X. S. Ren ◽  
T. M. Chang ◽  
W. Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Dependent Manner ◽  
Exocrine Pancreatic Secretion ◽  
Liquid Meal ◽  
Amylase Output ◽  
Endogenous Insulin

We have investigated a physiological role of endogenous insulin on exocrine pancreatic secretion stimulated by a liquid meal as well as exogenous secretin and cholecystokinin octapeptide (CCK-8) in conscious rats. Each rat was prepared with a chronic pancreatic fistula and an indwelling catheter in a jugular vein. Oral ingestion of a liquid meal (5 ml) resulted in significant increases in pancreatic secretion, including volume, bicarbonate, and amylase output, in these rats. A rabbit anti-insulin serum (1.0 ml) given intravenously completely blocked the postprandial exocrine pancreatic secretion, whereas a normal rabbit serum did not influence the pancreatic secretion in the same rats. When pancreatic secretion was stimulated by intravenous administration of both secretin and CCK-8 in three different doses, including 0.015, 0.03, and 0.06 clinical unit and microgram.kg-1.h-1, respectively, volume, bicarbonate, and amylase output increased significantly in a dose-dependent manner. This increase in pancreatic secretion was also completely blocked by a rabbit anti-insulin serum, whereas it was not influenced by a normal rabbit serum. The amount of the antiserum employed abolished the postprandial increases in plasma insulin concentration. We conclude that endogenous insulin plays an important role on the regulation of postprandial pancreatic secretion in rats. Furthermore, for the stimulatory action of the two intestinal hormones secretin and CCK-8 on the pancreatic exocrine secretion, endogenous insulin is need.

Inhibition of exocrine pancreatic secretion in dog by peptide YY is mediated by PYY-preferring Y2 receptors

1992 ◽  
Vol 40 (2) ◽  
pp. 162
Author(s):  
D Grandt ◽  
S Teyssen ◽  
M Schimiczek ◽  
E Niebergall ◽  
H Goebell ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Peptide Yy ◽  
Exocrine Pancreatic Secretion

Plasma secretin concentrations in fasting and postprandial states in dog.

1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Fasting State ◽  
Meat Meal ◽  
Duodenal Ph ◽  
The Mean ◽  
Bicarbonate Output ◽  
Marked Suppression ◽  
Sustained Increase

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.

On the Role of Gastrin-Releasing Peptide in Meal-Stimulated Exocrine Pancreatic Secretion

Pancreas ◽  
1999 ◽  
Vol 19 (2) ◽  
pp. 126-132 ◽  
Author(s):  
Olaf Horstmann ◽  
Rainer Nustede ◽  
Wolfgang Schmidt ◽  
Fritz Stöckmann ◽  
Heinz Becker
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Gastrin Releasing Peptide

Mutual dependence of VIP/PACAP and CCK receptor signaling for a physiological role in duck exocrine pancreatic secretion

2004 ◽  
Vol 286 (1) ◽  
pp. R189-R198 ◽  
Author(s):  
Rui Xiao ◽  
Zong Jie Cui
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Amylase Secretion ◽  
Maximal Effect ◽  
Exocrine Pancreatic Secretion ◽  
Pancreatic Acini ◽  
Vpac Receptors ◽  
Intracellular Ca ◽  
Protein Kinase C Inhibitor ◽  
Sensitizing Effect

Unlike in rodents, CCK has not been established as a physiological regulator in avian exocrine pancreatic secretion. In the isolated duck pancreatic acini, 1 nM CCK was required for stimulation of amylase secretion, maximal effect being achieved at 10 nM; picomolar CCK was without effect. Vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase activating peptide (PACAP) receptor (VPAC) agonists PACAP-38 and PACAP-27 (10-12-10-7 M) alone had no effect, but made picomolar CCK effective. VPAC agonist VIP 10-10-10-7 M stimulated amylase secretion marginally, but made CCK 10-12-10-10 M effective also. PACAP-27 and VIP both shifted the maximal CCK concentration from 10-8 to 10-9 M. This sensitizing effect was mimicked by forskolin. CCK dose dependently induced intracellular Ca2+ concentration ([Ca2+]i) oscillations. PACAP-38 (1 nM), PACAP-27 (1 nM), VIP (10 nM), or forskolin (10 μM) alone did not stimulate [Ca2+]i increase, neither did they modulate CCK (1 nM)-induced oscillations; but when they were added to cells simultaneously exposed to subthreshold CCK (10 pM), calcium spikes emerged. Amylase secretion induced by the simultaneous presence of 10 pM CCK and VPAC agonists was completely blocked by removing extracellular calcium, but the protein kinase C inhibitor staurosporine (1 μM) was without effect. CCK (10 nM)-induced secretion was inhibited by CCK1 receptor antagonist FK480 (1 μM). Gastrin from 10-12 to 10-6 M did not stimulate amylase secretion nor did it (100 nM) induce [Ca2+]i increase. The above data suggest that duck pancreatic acini possess both CCK1 and VPAC receptors; simultaneous activation of both is required for each to play a physiological role.

scholarly journals Pancreatic polypeptide release: Role of stimulants of exocrine pancreatic secretion in dogs

1984 ◽  
Vol 87 (3) ◽  
pp. 530-536 ◽  
Author(s):  
Christoph Beglinger ◽  
Ian L. Taylor ◽  
Morton I. Grossman ◽  
Travis E. Solomon
Keyword(s):  
Pancreatic Polypeptide ◽  
Pancreatic Secretion ◽  
Exocrine Pancreatic Secretion

Gastrin is not a physiological regulator of pancreatic exocrine secretion in the dog

1987 ◽  
Vol 252 (1) ◽  
pp. G40-G44
Author(s):  
E. Kohler ◽  
C. Beglinger ◽  
V. Eysselein ◽  
U. Grotzinger ◽  
K. Gyr
Keyword(s):  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Exocrine Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Response Curves ◽  
Blood Concentrations ◽  
Pancreatic Enzyme Secretion ◽  
Pancreatic Exocrine ◽  
Bicarbonate Output

The role of gastrin as a regulator of exocrine pancreatic secretion has not been proven adequately. In the present study we therefore compared the relative molar potencies of sulfated and unsulfated gastrin 17 with structurally related CCK peptides (synthetic CCK-8 and natural porcine CCK-33) in stimulating exocrine pancreatic secretion in conscious dogs. Dose response curves were constructed for pancreatic and gastric acid secretion. Plasma gastrin levels after exogenous gastrin 17-I and -II were compared with postprandial gastrin concentrations (meal: ground beef 20 g/kg body wt). The molar potency estimates calculated with synthetic CCK8 as standard (potency = 1.00) for pancreatic protein secretion were natural porcine 50% pure CCK-33 1.60, gastrin 17-I 0.12, and gastrin 17-II 0.16. All four peptides induced a dose-dependent increase in pancreatic bicarbonate output. However, the blood concentrations needed to stimulate pancreatic secretion were above the postprandial gastrin levels. Our data indicate that both gastrin 17 peptides are not physiological regulators of pancreatic enzyme secretion in dogs.

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