Effect of equimolar amounts of long-chain triglycerides and medium-chain triglycerides on plasma cholecystokinin and gallbladder contraction

Hopman, W. P. M.; Jansen, J. B. M. J.; Rosenbusch, Gerd; Lamers, C. B. H. W.

doi:10.1093/ajcn/39.3.356

Cited by 83 publications

(46 citation statements)

References 17 publications

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“…Our observation that medium-chain triglycerides do not stimulate cholecystokinin secretion is in agreement with previous findings. 5 We conclude that intraduodenal infusion of long-chain triglycerides does not affect small-bowel transit time, although it significantly increases cholecystoldnin secre tion, whereas infusion of medium-chain triglycerides significantly accelerates small-bowel transit time, inde pendent of cholecystoldnin.…”

Section: Jannary-fcbruary 1995mentioning

confidence: 62%

Effect of Equimolar Amounts of Long‐Chain Triglycerides and Medium‐Chain Triglycerides on Small‐Bowel Transit Time in Humans

Ledeboer

Masclee

Jansen³

et al. 1995

J Parenter Enteral Nutr

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Section: Jannary-fcbruary 1995mentioning

confidence: 62%

Effect of Equimolar Amounts of Long‐Chain Triglycerides and Medium‐Chain Triglycerides on Small‐Bowel Transit Time in Humans

Ledeboer

Masclee

Jansen³

et al. 1995

J Parenter Enteral Nutr

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“…CCK is released from the upper small intestinal mucosa after ingestion of meals [6,8,9,13,18]. Because several investigators found good correlations between gallbladder contraction and plasma CCK levels in response to meals, and be cause infusion of CCK to levels comparable to those found after meals induced similar gallbladder responses, there is strong evi dence for this effect to be mediated by the release of CCK [5,6,9,11,13,14], Gallblad der contraction to all forms of physiological stimulation studied until now was accompa nied by increases in plasma CCK. However, this study showed that cephalic stimulation of gallbladder contraction by an appetizing meal did not induce release of CCK into the circulation.…”

Section: Discussionmentioning

confidence: 99%

Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

Hopman¹,

Jansen²,

Rosenbusch³

1987

Digestion

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To determine the role of cholecystokinin and the cholinergic system in cephalic stimulation of gallbladder contraction and to compare the degree of gallbladder contraction by cephalic stimulation with postprandial gallbladder contraction, 8 healthy volunteers (4 males, 4 females, 20–65 years) underwent the following studies: sham feeding of an appetizing meal, sham feeding with intravenous atropine, and ingestion of the same meal. Gallbladder volume was measured by real-time ultrasonography and plasma cholecystokinin by a sensitive and specific radioimmunoassay using antibody T204. Gallbladder contraction in response to sham feeding, 30 ± 4% (p = 0.0001 vs. basal), amounted to half of that seen after real feeding, 69 ± 5% (p < 0.0001 vs. basal). Significant dissociation between gallbladder response to sham feeding and real feeding was seen from 40 min (p < 0.005-p = 0.0001). Atropine did not affect basal gallbladder volume but completely abolished gallbladder contraction in response to sham feeding. Neither sham feeding without nor sham feeding with atropine significantly affected plasma cholecystokinin levels. On the other hand, real feeding induced significant increases in plasma cholecystokinin from a basal level of 2.3 ± 0.1 pM to a peak value of 5.9 ± 0.4 pM at 40 min. It is concluded that an important cephalic phase of postprandial gallbladder contraction exists which is cholecystokinin-independent but dependent on a cholinergic mechanism.

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“…Porcine intestinal DBI could also stimulate CCK release when administered intraduodenally in rat (47). The biologically active DBI fragment DBI (33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50) induces Ca 2ϩ oscillations and CCK secretion in STC-1 cells (151). In addition to luminal factors, neuropeptide bombesin (101,131,136), ␤-adrenergic receptor agonist (127), GABA (44,54), and orexins (69) could all stimulate I cell CCK secretion.…”

Section: Gut Cck-secreting Cellmentioning

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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Effect of equimolar amounts of long-chain triglycerides and medium-chain triglycerides on plasma cholecystokinin and gallbladder contraction

Cited by 83 publications

References 17 publications

Effect of Equimolar Amounts of Long‐Chain Triglycerides and Medium‐Chain Triglycerides on Small‐Bowel Transit Time in Humans

Effect of Equimolar Amounts of Long‐Chain Triglycerides and Medium‐Chain Triglycerides on Small‐Bowel Transit Time in Humans

Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

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

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