Physiological plasma concentrations of cholecystokinin stimulate pancreatic enzyme secretion and gallbladder contraction in man

Kerstens, P.J.S.M.; Lamers, C. B. H. W.; Jansen, J. B. M. J.; Jong, A. J. L. De; Hessels, M.; Hafkenscheid, J. C. M.

doi:10.1016/0024-3205(85)90638-1

Cited by 58 publications

(19 citation statements)

References 12 publications

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“…Recent investigations have shown that administration of the CCK analogue cerulein in concentrations mimicking post prandial plasma values of CCK. cause a sig nificant release of pancreatic enzymes in man [37,38]. In our study, gastric distension evoked plasma CCK concentrations which can at least in part account for distensioninduced pancreatic enzyme discharge ob served in previous studies [9], Inhibition of distension-induced enzyme release by atro pine does not invalidate the role of CCK under these conditions, since CCK release was also blocked by atropine.…”

Section: Discussionmentioning

confidence: 56%

Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Koop

Ruppert-Seipp²,

Koop³

et al. 1990

Digestion

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The effect of gastric distension on plasma cholecystokinin (CCK), pancreatic polypeptide (PP) and gastrin concentrations was investigated in healthy volunteers. Fundic and antral distension was achieved by balloons attached to a gastric tube and inflated with 300 and 600 ml and 100 and 200 ml of air for fundic and antral distension, respectively. Gastric juice was continuously aspirated. Fundic distension was additionally studied during a concomitant intravenous infusion of atropine (5 µg/kg/h) or a bolus injection of propranolol (2 mg). Fundic distension with 300 ml caused a significant increase in PP release (+ 17% above basal). Distension with 600 ml significantly stimulated CCK (+ 81 %), gastrin (+ 31 %) and PP output (+ 74%) over 30 min. Atropine completely blocked PP release and almost abolished CCK release, whereas gastrin output was enhanced. Propranolol did not prevent CCK release induced by fundic distension, whereas gastrin and PP responses were diminished. Antral distension did not cause any significant changes in hormone response. In conclusion, we demonstrated a gastric phase of CCK release which is atropine sensitive, but not influenced by propranolol.

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Section: Discussionmentioning

confidence: 56%

Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Koop

Ruppert-Seipp²,

Koop³

et al. 1990

Digestion

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“…Digestible fat is a powerfu 1 stiinu 1 us for plasma cholecysto kinin (CCK) release and subsequently for gallbladder contrac tion and pancreatic enzyme secretion (11)(12)(13)(14)(15)(16)(17). It has been suggested that the inhibition of gastric acid secretion is also mediated at least in part by CCK (8)(9)(10)(18)(19)(20)(21)(22).…”

Section: Introduction Materialsmentioning

confidence: 99%

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men

Maas

Hopman

Wijk

et al. 1997

The American Journal of Clinical Nutrition

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Replacement of dietary lilt by sucrose polyester reduces fat intake. However, little is known about the effccts of sucrose polyester on gastrointestinal function. To investigate the effect on gastric acid secretion and on release of cholecystokinin into plasma, we perfused eight healthy male volunteers intraduodenally with sucrose polyester, digestible fat, or saline on separate days in random order, Intraduodenal perfusion of sucrose polyester did not suppress gastrin-stimulated gastric acid secretion ( -1.8 ± 6,8%) whereas digestible fat suppressed gastric acid secretion by 64 ± 9% (P = 0.001) compared with saline. Sucrose polyester did not affect plasma cholecystokinin concentrations (-12.8 ± 9.3 pmol • 30 min/L) whereas perfusion with digestible fat resulted in a significant increase (31.7 ± 9.3 pmol -30 min/L, P ~ 0,017) compared with saline. We conclude that sucrose polyester, in contrast with digestible fat, does not inhibit gastrin-stimulated gastric acid secretion or stimulate release of cholecystokinin, KEY WORDS cholecystokininGastric acid secretion, sucrose polyester, Stimulation of plasma CCK and pancreaticobiliary secretion by fatty nutrients depends on the presence of the products of fat digestion in the proximal small intestine (23-29). The inhibi tion of gastric acid secretion by fat might dopend on (he digestion of fat as well.We report the effect of digestible fat and the indigestible fat sucrose polyester on gastric acid secretion and on CCK release in men.

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“…pancreatic acinar cells; vagal afferent nerves; plasma cholecystokinin concentration; species specificity IT IS GENERALLY ACCEPTED THAT cholecystokinin (CCK) as a gut hormone is an important endogenous secretagogue in exocrine pancreatic secretion. CCK also stimulates gallbladder contraction and enhances growth of the exocrine pancreas (63,115,138). CCK is produced and released by the intestinal mucosal I cells (78).…”

mentioning

confidence: 99%

“…CCK also stimulates gallbladder contraction and enhances growth of the exocrine pancreas (63,115,138). CCK is produced and released by the intestinal mucosal I cells (78).…”

mentioning

confidence: 99%

How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans

Wang¹,

Cui²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Wang BJ, Cui ZJ. How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans. Am J Physiol Regul Integr Comp Physiol 292: R666-R678, 2007. First published October 19, 2006; doi:10.1152/ajpregu.00131.2006.-The field of cholecystokinin (CCK) stimulation of exocrine pancreatic secretion has experienced major changes in the recent past. This review attempts to summarize the present status of the field. CCK production in the intestinal I cells, the molecular forms of CCK produced and subsequently circulated in the blood, the presence or absence of CCK receptors on the isolated pancreatic acinar cells and the associated signaling for acinar cell secretion, and the actual circuits and sites of action for CCK regulation of exocrine pancreatic secretion in vivo are reviewed in different animal species with an emphasis on birds, rodents, and humans. Clear differences in the relative importance of neural and direct modes of CCK action on pancreatic acinar cells were identified. Rodents seem to be endowed with both modes of action, whereas in humans the neural mode may predominate. In birds, such as duck, the direct mode needs further assistance from pituitary adenylate cyclaseactivating peptide/VIP receptors. However, much further work needs to be directed to the neural mode to map out all sites of CCK action and details of the full circuits, and we foresee a major revival for this field of research in the near future. pancreatic acinar cells; vagal afferent nerves; plasma cholecystokinin concentration; species specificity IT IS GENERALLY ACCEPTED THAT cholecystokinin (CCK) as a gut hormone is an important endogenous secretagogue in exocrine pancreatic secretion. CCK also stimulates gallbladder contraction and enhances growth of the exocrine pancreas (63,115,138). CCK is produced and released by the intestinal mucosal I cells (78). This source of CCK may travel through the circulation to target tissues that include the exocrine pancreas and gallbladder (65,78). CCK peptides are also found in large quantities in neurons, but neuronal CCK contributes negligibly to CCK concentration in the circulation (118). This general picture has been changed drastically by the recent findings that CCK can also stimulate exocrine pancreatic secretion by the excitation of sensory nerves and vagovagal and enteropancreatic reflexes, and this may be the only pathway in humans (65, 105). In addition, major differences have been found in the traditional humoral pathway, depending on the animal species (35,149). Therefore, the purpose of this review is to present the current status of CCK regulation of exocrine pancreatic secretion with a particular emphasis on species specificity as shown in birds, rodents, and humans.

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Physiological plasma concentrations of cholecystokinin stimulate pancreatic enzyme secretion and gallbladder contraction in man

Cited by 58 publications

References 12 publications

Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men

How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans

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