Comparative effects of CCK-8 on feeding, sham feeding, and exocrine pancreatic secretion in rats

1986 ◽  
Vol 251 (1) ◽  
pp. R97-R105 ◽  
Author(s):  
R. D. Reidelberger ◽  
T. E. Solomon
Keyword(s):  
Food Intake ◽  
Pancreatic Secretion ◽  
Gastric Distension ◽  
Exocrine Pancreatic Secretion ◽  
Humoral Factors ◽  
Sham Feeding ◽  
Hormonal Mechanism ◽  
Satiety Hormone ◽  
Feeding Effect ◽  
Normal Feeding

Cholecystokinin (CCK) is thought to be a hormonal regulator of exocrine pancreatic secretion and is postulated to be a satiety hormone. We compared the dose-response effects of CCK octapeptide (CCK-8) on feeding, sham feeding, and pancreatic secretion to gauge whether the feeding effect might be physiological. Pancreatic responses to intravenous CCK-8 (40, 200, 1,000, or 4,000 pmol . kg-1 . h-1) in fasted unanesthetized rats were compared with effects of CCK-8 (0, 200, 1,000, or 4,000 pmol . kg-1 . h-1) on ingestion of liquid diet in fasted rats with gastric cannulas either closed (normal feeding) or open (sham feeding). Maximal pancreatic amylase output occurred at 200 pmol . kg-1 . h-1 of CCK-8; output declined at higher doses. Food intake was significantly inhibited only at 1,000 and 4,000 pmol . kg-1 . h-1 of CCK-8; the effect was similar when gastric cannulas were closed and open. These results, together with available data on the low postprandial levels of plasma CCK, suggest that circulating levels of CCK normally present after food intake are not sufficient to produce satiety. Furthermore, suppression of feeding by CCK does not appear to be mediated solely by a mechanism that senses gastric distension, because CCK-8 had similar effects in the presence and absence of gastric distension. Whether CCK interacts with other neural or humoral factors to produce satiety by a hormonal mechanism remains to be determined.

Cholecystokinin receptors and vagal nerves in control of food intake in rats

1990 ◽  
Vol 258 (1) ◽  
pp. E40-E45 ◽  
Author(s):  
J. Garlicki ◽  
P. K. Konturek ◽  
J. Majka ◽  
N. Kwiecien ◽  
S. J. Konturek
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Gastric Inhibitory Polypeptide ◽  
Intragastric Administration ◽  
Gut Peptides ◽  
Sham Feeding ◽  
Liquid Meal ◽  
Vagal Nerves ◽  
Normal Feeding ◽  
Cck Receptor Antagonist

This study was designed to determine the specificity and physiological nature of short-term satiety effects of cholecystokinin (CCK) in rats with intact and transected vagal nerves. Rats with-the gastric fistulas, closed or open, were used for normal feeding or sham feeding of liquid meal offered for 30 min. CCK-8 (0.5-10 nmol/kg) injected intraperitoneally (ip) 15 min before feeding inhibited food intake dose dependently in both normal-fed and sham-fed rats at a minimal inhibitory dose of 1 nmol/kg. CCK-8 at the same doses caused a potent stimulation of pancreatic protein secretion, reaching maximum at a dose of approximately 0.5 nmol/kg. Pretreatment with a potent CCK receptor antagonist, L-364,718 (2.5 mg/kg ip), increased food intake during normal feeding (but not sham feeding) and almost completely blocked the satiety and pancreatic stimulatory effects of CCK. When feeding was preceded by intragastric administration of proteinase inhibitor (Foy-305, 200 mg/kg), food preload, or diversion of bile-pancreatic secretion to the exterior, there was a significant increase in the plasma level of CCK and an inhibition of food intake by about 36, 78, and 25%, respectively. Pretreatment with L-364,718 completely abolished this inhibition by Foy-305 and bile-pancreatic diversion and reduced that caused by food preload. Among other gut peptides given ip (10 nmol/kg) only bombesin reduced food intake, whereas gastrin, secretin, gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), and peptide YY (PYY) were ineffective.(ABSTRACT TRUNCATED AT 250 WORDS)

Serotonin type-3 receptors mediate cholecystokinin-induced satiation through gastric distension

2006 ◽  
Vol 291 (1) ◽  
pp. R115-R123 ◽  
Author(s):  
Matthew R. Hayes ◽  
Fiona M. Chory ◽  
Claire A. Gallagher ◽  
Mihai Covasa
Keyword(s):  
Food Intake ◽  
Gastric Distension ◽  
Sucrose Intake ◽  
Gastric Balloon ◽  
Sham Feeding ◽  
Balloon Distension ◽  
Type 3

We have previously shown that serotonin type-3 (5-HT3) receptors mediate cholecystokinin (CCK)-induced satiation and that this effect is dependent on postoropharyngeal feedback. However, the independent contributions of gastric and intestinal feedback in 5-HT3 receptor mediation of suppression of food intake by CCK have not been determined. Using a sham-feeding preparation combined with intraduodenal sucrose infusion, we show that blockade of 5-HT3 receptors by ondansetron (1 mg/kg ip) had no effect on suppression of sham feeding by intraduodenal 15% sucrose infusion (4 ml/10 min), CCK (2 μg/kg ip) administration, or the combination of the two treatments. In separate experiments consisting of either sham-feeding rats that received gastric distension with the use of a balloon or real-feeding rats whose stomachs were distended using gastric loads of saline after the occlusion of the pylorus, we tested the hypothesis that gastric feedback signals are necessary for activation of 5-HT3 receptors. Ondansetron significantly attenuated suppression of sham sucrose intake after a 10-ml gastric balloon distension (30.5 ± 2.2 vs. 20.2 ± 2.2 ml, respectively) and gastric distension combined with CCK (21.9 ± 1.4 vs. 12.0 ± 1.7 ml, respectively). When intestinal feedback was eliminated in a real-feeding paradigm by closing the pylorus using a cuff preparation, ondansetron attenuated suppression of sucrose intake produced by a 10-ml saline gastric load (6.8 ± 0.7 vs. 4.2 ± 0.4 ml, respectively). Finally, when CCK (1 μg/kg) was administered in combination with a 5-ml saline gastric load in a real-feeding preparation, ondansetron significantly attenuated suppression of sucrose intake by CCK (9.0 ± 0.9 vs. 6.3 ± 0.5 ml, respectively), as well as the enhanced suppression of intake by CCK plus gastric load (6.9 ± 0.6 vs. 4.6 ± 0.5 ml, respectively). These findings demonstrate that CCK-induced activation of 5-HT3 receptors requires gastric, but not intestinal feedback.

Pancreatic secretory response to feeding in the calf: CCK-A receptors, but not CCK-B/gastrin receptors are involved

2000 ◽  
Vol 78 (10) ◽  
pp. 813-819 ◽  
Author(s):  
Gwenola Le Dréan ◽  
Isabelle Le Huërou-Luron ◽  
Martine Gestin ◽  
Véronique Romé ◽  
Christine Bernard ◽  
...  
Keyword(s):  
Food Intake ◽  
Pancreatic Juice ◽  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Neural Pathways ◽  
Enzyme Release ◽  
Exocrine Pancreatic Secretion ◽  
External Stimuli ◽  
Bovine Species

In bovine species, as in human, the pancreas predominantly expresses cholecystokinin-B (CCK-B)/gastrin receptors. However, the role of this receptor in the regulation of meal-stimulated pancreatic enzyme release has not been determined. In milk-fed calves, we previously described prandial patterns of exocrine pancreatic secretion and a long prefeeding phase was observed. The present study was aimed at determining both the role of external stimuli in the outset of the prefeeding phase and the implication of pancreatic CCK-A and CCK-B/gastrin receptors in the mediation of pancreatic response to feeding. The first objective was studied by suppressing external stimuli associated with food intake (unexpected meal) and the second by infusing highly specific and potent antagonists of CCK-A (SR 27897) and CCK-B/gastrin (PD 135158) receptors during the prandial period. When calves were given an unexpected meal, the long prefeeding increase in pancreatic secretion was absent. SR 27897 (but not PD 135158) inhibited the preprandial phase and greatly reduced postprandial pancreatic juice and enzyme outflows. The expectancy of a meal seemed to elicit an increased pancreatic response right before a meal and CCK-A receptors may mediate this information via neural pathways. The implication of CCK and CCK-A receptors in mediating the postfeeding pancreatic response was also demonstrated. The participation of CCK-B/gastrin receptors in this regulation was not demonstrated.Key words: CCK-A and CCK-B/gastrin receptors, cholecystokinin, exocrine pancreatic secretion, feeding, milk-fed calf.

Interaction of GLP-1 with gastric distension in regulating food intake and satiety in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A208-A208
Author(s):  
L DEGEN ◽  
D MATZINGER ◽  
B FISCHER ◽  
F ZIMMERLI ◽  
M KNUPP ◽  
...  
Keyword(s):  
Food Intake ◽  
Gastric Distension

The effect of stress conditions on exocrine pancreatic secretion in growing pigs

1999 ◽  
Vol 82 (4) ◽  
pp. 150-162 ◽  
Author(s):  
J. A. M. Botermans ◽  
J. Svendsen ◽  
B. R. Westrom ◽  
S. G. Pierzynowski
Keyword(s):  
Pancreatic Secretion ◽  
Growing Pigs ◽  
Stress Conditions ◽  
Exocrine Pancreatic Secretion

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

Mnk1 is a novel acinar cell-specific kinase required for exocrine pancreatic secretion and response to pancreatitis in mice

Gut ◽  
2014 ◽  
Vol 64 (6) ◽  
pp. 937-947 ◽  
Author(s):  
Jaroslaw Cendrowski ◽  
Víctor J Sánchez-Arévalo Lobo ◽  
Matthias Sendler ◽  
Antonio Salas ◽  
Jens-Peter Kühn ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Pancreatic Secretion ◽  
Exocrine Pancreatic Secretion

Gastrin-Releasing Peptide and Cholecystokinin in the Regulation of Exocrine Pancreatic Secretion in Dogs

Digestion ◽  
1993 ◽  
Vol 54 (2) ◽  
pp. 79-83 ◽  
Author(s):  
Rainer Nustede ◽  
Wolfgang E. Schmidt ◽  
Christoph Lohmann ◽  
Heinz Köhler ◽  
Rolf Schlemminger ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Gastrin Releasing Peptide

Cholecystokinin is a Satiety Hormone in Humans at Physiological Post-Prandial Plasma Concentrations

1995 ◽  
Vol 89 (4) ◽  
pp. 375-381 ◽  
Author(s):  
Anne Ballinger ◽  
Lorraine McLoughlin ◽  
Sami Medbak ◽  
Michael Clark
Keyword(s):  
Food Intake ◽  
Test Meal ◽  
Plasma Concentrations ◽  
Standard Test ◽  
Saline Infusion ◽  
Reduce Food Intake ◽  
Subsequent Test ◽  
Gut Hormone ◽  
Plasma Cholecystokinin ◽  
Satiety Hormone

1. Intravenous infusions of the brain/gut hormone, cholecystokinin, have been shown to reduce food intake in a subsequent test meal. However, in previous studies the doses administered were large and likely to have produced plasma concentrations far in excess of the normal post-prandial range. 2. In this study cholecystokinin-8 was infused intravenously to six healthy subjects in doses that reproduced physiological post-prandial concentrations. Plasma concentrations of cholecystokinin were measured using a novel sensitive and specific radioimmunoassay. The effect of cholecystokinin-8 infusion on subsequent food intake in a standard test meal was compared with the effect of saline infusion in the same subjects. 3. Food intake (mean ± SEM) was significantly less during cholecystokinin (5092 ± 665 kJ) than during saline infusion (6418 ± 723 kJ, P = 0.03). During cholecystokinin infusion, plasma concentrations increased from 0.45 ± 0.06 pmol/l to 7.28 ± 2.43 pmol/l immediately before the meal. With saline infusion there was no premeal increase in plasma cholecystokinin concentration. 4. This paper describes a novel radioimmunoassay for measurement of plasma concentrations of cholecystokinin. Using this assay we have demonstrated that cholecystokinin is important in control of satiety in humans.

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