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.

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

Central administration of alpha-MSH antiserum augments fever in the rabbit

1986 ◽  
Vol 250 (5) ◽  
pp. R803-R806 ◽  
Author(s):  
S. T. Shih ◽  
O. Khorram ◽  
J. M. Lipton ◽  
S. M. McCann
Keyword(s):  
Interleukin 1 ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Central Administration ◽  
Normal Body Temperature ◽  
Melanocyte Stimulating Hormone ◽  
Average Rise ◽  
The Brain ◽  
Antipyretic Action

alpha-Melanocyte-stimulating hormone (alpha-MSH) has a marked antipyretic action when given centrally or peripherally, and the concentration of this peptide within the septal region of the brain increases during fever. To assess the significance of endogenous central alpha-MSH in fever, antiserum was given to rabbits via a cannula implanted in the third cerebral ventricle. Each day for 3 days, the animals received 50 microliters of normal rabbit serum (NRS) or an equal volume of antiserum raised against alpha-MSH. Interleukin 1 (IL 1) was then injected intravenously to determine the effect of central immunoneutralization of alpha-MSH on the febrile response. Immunoneutralization markedly prolonged fever. The average rise in temperature and the area under the fever curve after IL 1 injection were also significantly increased. Antiserum treatment did not alter normal body temperature, and NRS had no effect on IL 1-induced fever. These results indicate that endogenous central alpha-MSH contributes to physiological limitation of fever and that the role of this peptide in temperature regulation is relevant to the febrile state but not to normothermia.

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.

Inactivation of White Spot Syndrome Virus (WSSV) by normal rabbit serum: Implications for the role of the envelope protein VP28 in WSSV infection of shrimp

2006 ◽  
Vol 118 (1-2) ◽  
pp. 55-61 ◽  
Author(s):  
Javier Robalino ◽  
Caroline Payne ◽  
Pamela Parnell ◽  
Eleanor Shepard ◽  
Adrian C. Grimes ◽  
...  
Keyword(s):  
Envelope Protein ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
White Spot Syndrome

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 MEK inhibits secretin release and pancreatic secretion: roles of secretin-releasing peptide and somatostatin

2001 ◽  
Vol 280 (5) ◽  
pp. G890-G896 ◽  
Author(s):  
James P. Li ◽  
Kae Yol Lee ◽  
Ta-Min Chang ◽  
William Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Inhibitory Effect ◽  
Exocrine Secretion ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Pancreatic Exocrine Secretion ◽  
Pancreatic Fluid ◽  
Pancreatic Exocrine ◽  
Small Intestinal ◽  
Secretin Release

We investigated the mechanism of action of methionine enkephalin (MEK) on HCl-stimulated secretin release and pancreatic exocrine secretion. Anesthetized rats with pancreatobiliary cannulas and isolated upper small intestinal loops were perfused intraduodenally with 0.01 N HCl while bile and pancreatic juice were diverted. The effect of intravenous MEK on acid-stimulated secretin release and pancreatic exocrine secretion was then studied with or without coinfusion of naloxone, an anti-somatostatin (SS) serum, or normal rabbit serum. Duodenal acid perfusate, which contains secretin-releasing peptide (SRP) activity, was collected from donor rats with or without pretreatment with MEK, MEK + naloxone, or MEK + anti-SS serum, concentrated by ultrafiltration, and neutralized. The concentrated acid perfusate (CAP), which contains SRP bioactivity, was infused intraduodenally into recipient rats. MEK increased plasma SS concentration and inhibited secretin release and pancreatic fluid and bicarbonate secretion dose-dependently. The inhibition was partially reversed by naloxone and anti-SS serum but not by normal rabbit serum. In recipient rats, CAP increased plasma secretin level and pancreatic secretion. CAP SRP bioactivity decreased when it was collected from MEK-treated donor rats; this was partially reversed by coinfusion with naloxone or anti-SS serum. These results suggest that in the rat, MEK inhibition of acid-stimulated pancreatic secretion and secretin release involves suppression of SRP activity release. Thus the MEK inhibitory effect appears to be mediated in part by endogenous SS.

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