Role of cholecystokinin in intestinal phase and meal-induced pancreatic secretion

1989 ◽  
Vol 257 (5) ◽  
pp. G782-G790 ◽  
Author(s):  
W. E. Dale ◽  
C. M. Turkelson ◽  
T. E. Solomon
Keyword(s):  
Sodium Oleate ◽  
Pancreatic Secretion ◽  
Plasma Concentrations ◽  
Amylase Secretion ◽  
Bicarbonate Secretion ◽  
Lower Plasma ◽  
Intestinal Phase ◽  
Meat Meal ◽  
Plasma Cholecystokinin

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.

Effect of exocrine pancreatic secretagogues on circulating somatostatin in dogs

1986 ◽  
Vol 250 (1) ◽  
pp. G15-G20
Author(s):  
C. Beglinger ◽  
G. Ribes ◽  
I. Whitehouse ◽  
M. M. Loubatieres-Mariani ◽  
U. Grotzinger ◽  
...  
Keyword(s):  
Protein Secretion ◽  
Sodium Oleate ◽  
Pancreatic Secretion ◽  
Cell Function ◽  
Bicarbonate Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Intestinal Phase ◽  
Pancreatic Fistulas ◽  
D Cell ◽  
Quantitative Importance

Several secretagogues of exocrine pancreatic secretion have been proposed to act as regulators of pancreatic D-cell function. To characterize this relationship, we measured incremental responses of protein, bicarbonate, and circulating somatostatin to graded doses of intravenous cholecystokinin (CCK-33), CCK-8, caerulein, bombesin, secretin, and intraduodenally perfused HCl, sodium oleate, and L-phenylalanine in conscious dogs with gastric and pancreatic fistulas and compared them with postprandial values (to a beef meal). Bombesin produced dose-related increases in somatostatin secretion (maximal, 46% of meal response), but caerulein, CCK-33, and CCK-8 released only small amounts of somatostatin at doses equivalent for pancreatic protein secretion. Secretin did not stimulate somatostatin release at any dose studied, whereas intraduodenal HCl at a load submaximal for pancreatic bicarbonate secretion increased somatostatin levels slightly (maximal, 16% of meal response). L-Phenylalanine and sodium oleate markedly increased protein secretion, but only oleate clearly stimulated somatostatin release (maximal, 11% of meal response). Our results suggest a greater quantitative importance of the intestinal phase for exocrine pancreatic stimulation than for somatostatin release.

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.

Role of endogenous cholecystokinin on vagally stimulated pancreatic secretion in dogs

1989 ◽  
Vol 257 (6) ◽  
pp. G944-G949
Author(s):  
C. K. Kim ◽  
K. Y. Lee ◽  
T. Wang ◽  
G. Sun ◽  
T. M. Chang ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Plasma Concentrations ◽  
Exocrine Secretion ◽  
Vagus Nerves ◽  
Pancreatic Acini ◽  
Venous Circulation ◽  
Gut Hormone ◽  
Pancreatic Exocrine ◽  
Cck Receptor Antagonist

Pancreatic exocrine secretion was evoked by electrical stimulation of the vagus nerves (EVS) in dogs to determine whether a gut hormone was responsible for the pancreatic stimulatory activity. In 39 dogs, pancreatic juice was continuously collected to measure volume, bicarbonate, and amylase output, while portal and femoral venous plasma concentrations of gastrin, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), and pancreatic polypeptide (PP) were determined by radioimmunoassay. EVS produced a significant increase in the pancreatic secretion. Although concentrations of all four peptides significantly increased in plasma, only CCK at the concentration in venous circulation was bioactive in dispersed rat pancreatic acini preparations. This bioactivity of CCK was completely blocked by CR 1409, a CCK-receptor antagonist. The pancreatic secretion by EVS was reduced significantly by intravenous MK-329 (formerly L364,718) to as low as 22% of control values and was completely suppressed by intravenous atropine. The increment in plasma CCK by EVS was also significantly suppressed by atropine. The present study indicates that increased pancreatic secretion by EVS is in part mediated by endogenous CCK.

Role of cholecystokinin in intestinal phase of human pancreatic secretion

1987 ◽  
Vol 32 (2) ◽  
pp. 155-163 ◽  
Author(s):  
William R. Brugge ◽  
Catherine A. Burke ◽  
Richard S. Izzo ◽  
Melvin Praissman
Keyword(s):  
Pancreatic Secretion ◽  
Intestinal Phase

Plasma secretin, CCK, and pancreatic secretion in response to dietary fat in the rat

1989 ◽  
Vol 256 (6) ◽  
pp. G1016-G1021 ◽  
Author(s):  
G. M. Green ◽  
S. Taguchi ◽  
J. Friestman ◽  
W. Y. Chey ◽  
R. A. Liddle
Keyword(s):  
Protein Secretion ◽  
Trypsin Inhibitor ◽  
Dietary Fat ◽  
Pancreatic Secretion ◽  
Intraduodenal Infusion ◽  
Reduced Fat ◽  
Plasma Cholecystokinin ◽  
Protein Output ◽  
Secretin Release

The role of fat in regulation of pancreatic secretion was studied in conscious rats by measuring pancreatic secretion and plasma cholecystokinin (CCK) and secretin responses to intraluminal infusion of fat, protein, or trypsin inhibitor via the duodenum. In rats with pancreatic juice continuously returned to the intestine, intraduodenal infusion of 20% emulsified fat (Liposyn), 10% casein, and 0.4% ovomucoid trypsin inhibitor (OMTI) stimulated equivalent increases of approximately threefold in pancreatic protein output. Proglumide reduced fat-stimulated pancreatic protein secretion by greater than 90% but did not inhibit the response to OMTI. Fat significantly increased plasma CCK from basal levels of 0.5 pM to 2-3 pM, but it was a weaker stimulant of CCK secretion than casein (peak CCK levels greater than 10 pM) or OMTI (peak CCK levels 5-6 pM). Fat significantly stimulated secretin release (21.7 pM) compared with casein (6.8 pM), OMTI (4.4 pM), and NaCl (3.5 pM). The inhibition of fat-stimulated pancreatic secretion by proglumide indicates that the small amounts of CCK released by fat are necessary for a normal pancreatic response, suggesting that this response may be the result of potentiation between secretin and small amounts of CCK.

Biphasic secretory response of exocrine pancreas to feeding

1980 ◽  
Vol 238 (4) ◽  
pp. G332-G337 ◽  
Author(s):  
Z. Itoh ◽  
R. Honda ◽  
K. Hiwatashi
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreas ◽  
Physiological Role ◽  
Secretory Response ◽  
Conscious Dogs ◽  
Bicarbonate Secretion ◽  
Secretory Pattern ◽  
Second Peak

By means of a newly developed device, secretory response of the exocrine pancreas to feeding was continuously recorded for 24 h in conscious dogs. It was then found that the postprandial secretory pattern of the pancreas was biphasic. The first peak of secretion, rich in enzymes, occurred 2.3 +/- 0.11 h after feeding and its secretory volume was 25.3 +/- 3.10 ml/h. After the first peak, pancreatic secretion decreased slightly, but started to increase again. At 10.8 +/- 0.31 h after feeding, the second peak of secretion occurred and this was 40.5 +/- 2.93 ml/h, significantly higher than the first peak secretion and the greatest in 1 day. The second peak secretion did not contain a higher concentration of enzymes, but was rich in bicarbonate. Approximately 16 h after feeding, pancreatic secretion returned to the basal level, which continued until the next meal. That water and bicarbonate secretion of the pancreas is the greatest at about the 11th postprandial h had never been reported before. The physiological role of the pancreatic secretion at that time is more likely to be related to the neutralization of acid entering from the stomach than to the digestion of food.

Role of the small intestine and gastric antrum in pancreatic polypeptide release

1981 ◽  
Vol 240 (5) ◽  
pp. G387-G391
Author(s):  
I. L. Taylor ◽  
G. L. Kauffman ◽  
J. H. Walsh ◽  
H. Trout ◽  
P. Chew ◽  
...  
Keyword(s):  
Small Intestine ◽  
Pancreatic Polypeptide ◽  
Liver Extract ◽  
Inhibitory Effect ◽  
Gastric Antrum ◽  
Intestinal Phase ◽  
Meat Meal ◽  
Before And After ◽  
Gastrointestinal Peptides

Gastrointestinal peptides have been proposed to play an important role in the pancreatic polypeptide response to a meal. These studies examine the role of the small intestine and gastric antrum in pancreatic polypeptide release in unanesthetized dogs. Intestinal perfusion with 5% liver extract in seven dogs resulted in a significant increase (P less than 0.05) in serum pancreatic polypeptide concentration (mean delta PP = 35.0 +/- 10.5 pM). Antrectomy without truncal vagotomy in four of these dogs significantly inhibited (P less than 0.05) this response. In five other dogs, antrectomy inhibited the pancreatic polypeptide response to an ingested meat meal by 81.9 +/- 4.5% (P less than 0.01). To further delineate the mechanism by which antrectomy inhibits pancreatic polypeptide release, the pancreatic polypeptide response to a meal was measured in four dogs before and after selective antral denervation. Antral denervation inhibited pancreatic polypeptide release to a degree similar (81.5 +/- 13.4%) to that previously observed after antrectomy. These studies have demonstrated an intestinal phase of pancreatic polypeptide release. They also suggest that antrectomy exerts its inhibitory effect on pancreatic polypeptide release by partially denervating the pancreas.

scholarly journals The role of cGMP-cGKI-signaling for duodenal bicarbonate secretion

2009 ◽  
Vol 9 (S1) ◽  
Author(s):  
Beate Spiessberger ◽  
Pascal Weinmeister ◽  
Franz Hofmann ◽  
Claudia Werner ◽  
Dieter Saur ◽  
...  
Keyword(s):  
Bicarbonate Secretion ◽  
Duodenal Bicarbonate Secretion

scholarly journals Antioxidants Promote Intestinal Tumor Progression in Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 241
Author(s):  
Zhiyuan V. Zou ◽  
Kristell Le Gal ◽  
Ahmed E. El Zowalaty ◽  
Lara E. Pehlivanoglu ◽  
Viktor Garellick ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Tumor Progression ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Intestinal Tumor ◽  
Adenomatous Polyposis ◽  
Intestinal Tumors ◽  
The Impact

Dietary antioxidants and supplements are widely used to protect against cancer, even though it is now clear that antioxidants can promote tumor progression by helping cancer cells to overcome barriers of oxidative stress. Although recent studies have, in great detail, explored the role of antioxidants in lung and skin tumors driven by RAS and RAF mutations, little is known about the impact of antioxidant supplementation on other cancers, including Wnt-driven tumors originating from the gut. Here, we show that supplementation with the antioxidants N-acetylcysteine (NAC) and vitamin E promotes intestinal tumor progression in the ApcMin mouse model for familial adenomatous polyposis, a hereditary form of colorectal cancer, driven by Wnt signaling. Both antioxidants increased tumor size in early neoplasias and tumor grades in more advanced lesions without any impact on tumor initiation. Importantly, NAC treatment accelerated tumor progression at plasma concentrations comparable to those obtained in human subjects after prescription doses of the drug. These results demonstrate that antioxidants play an important role in the progression of intestinal tumors, which may have implications for patients with or predisposed to colorectal cancer.

scholarly journals Vitamin C—Sources, Physiological Role, Kinetics, Deficiency, Use, Toxicity, and Determination

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 615
Author(s):  
Martin Doseděl ◽  
Eduard Jirkovský ◽  
Kateřina Macáková ◽  
Lenka Krčmová ◽  
Lenka Javorská ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Iron Absorption ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Renal Stones ◽  
Anti Oxidant ◽  
High Doses ◽  
Epigenetic Processes

Vitamin C (L-ascorbic acid) has been known as an antioxidant for most people. However, its physiological role is much larger and encompasses very different processes ranging from facilitation of iron absorption through involvement in hormones and carnitine synthesis for important roles in epigenetic processes. Contrarily, high doses act as a pro-oxidant than an anti-oxidant. This may also be the reason why plasma levels are meticulously regulated on the level of absorption and excretion in the kidney. Interestingly, most cells contain vitamin C in millimolar concentrations, which is much higher than its plasma concentrations, and compared to other vitamins. The role of vitamin C is well demonstrated by miscellaneous symptoms of its absence—scurvy. The only clinically well-documented indication for vitamin C is scurvy. The effects of vitamin C administration on cancer, cardiovascular diseases, and infections are rather minor or even debatable in the general population. Vitamin C is relatively safe, but caution should be given to the administration of high doses, which can cause overt side effects in some susceptible patients (e.g., oxalate renal stones). Lastly, analytical methods for its determination with advantages and pitfalls are also discussed in this review.

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