Role of cholecystokinin in the regulation of gastric emptying and pancreatic enzyme secretion in humans

Fried, Michael; Erlacher, U.; Schwizer, Werner; Löchner, Christine; Koerfer, Joachim; Beglinger, Christoph; Jansen, J. B. M. J.; Lamers, C. B. H. W.; Harder, F.; Bischof-Delaloye, A.; Stalder, G; Rovati, Lucio C.

doi:10.1016/0016-5085(91)90031-f

Cited by 165 publications

(108 citation statements)

References 23 publications

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“…It stimulates gallbladder contraction and pancreatic enzyme secretion, and retards gastric emptying [82,83]. Furthermore, the release of PYY and GLP-1, after lipid ingestion, is dependent on signaling through the CCK receptor [84,85].…”

Section: Cholecystokininmentioning

confidence: 99%

Therapy for Obesity Based on Gastrointestinal Hormones

Christensen¹,

Knop²,

Vilsbøll³

2011

Rev Diabet Stud

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■ AbstractIt has long been known that peptide hormones from the gastrointestinal tract have significant impact on the regulation of nutrient metabolism. Among these hormones, incretins have been found to increase insulin secretion, and thus incretin-based therapies have emerged as new modalities for the treatment of type 2 diabetes. In contrast to other antidiabetic treatments, these agents have a positive outcome profile on body weight. Worldwide there are 500 million obese people, and 3 million are dying every year from obesityrelated diseases. Recently, incretin-based therapy was proposed for the treatment of obesity. Currently two different incretin therapies are widely used in the treatment of type 2 diabetes: 1) the GLP-1 receptor agonists which cause significant and sustained weight loss in overweight patients, and 2) dipeptidyl peptidase 4 (DPP-4) inhibitors being weight neutral. These findings have led to a greater interest in the physiology of intestinal peptides with potential weightreducing properties. This review discusses the effects of the incretin-based therapies in obesity, and provides an overview of intestinal peptides with promising effects as potential new treatments for obesity.

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Section: Cholecystokininmentioning

confidence: 99%

Therapy for Obesity Based on Gastrointestinal Hormones

Christensen¹,

Knop²,

Vilsbøll³

2011

Rev Diabet Stud

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“…First, even complete CCK-receptor blockade by a selective CCK-receptor an tagonist causes only moderate (about 40%) acceleration of human gastric emptying of a liquid mixed meal very similar to the one used by us. 48 It is unlikely that the comparatively small difference in CCK release observed in our study could have been the sole mechanism respon sible for the pronounced motor effects. Second, differ ences in CCK responses occurred within the first 2 post prandial hours when gastric emptying rates did not differ.…”

mentioning

confidence: 65%

“…in inducing and maintaining the fed state and to be a physiological inhibitor of gastric emptying. 48 We ob served that, in our patients with severe untreated pancreto enzyme therapy, atic insufficiency, CCK release in response to the liquid test meal was decreased but was restored by enzyme supplementation. These findings are explained by slower luminal generation of stimulatory digestion products and confirm earlier studies using different test meals.49-51 Thus, a diminished postprandial CCK response in pan creatic insufficiency accelerates gastric emptying.…”

mentioning

confidence: 81%

Altered postprandial motility in chronic pancreatitis: Role of malabsorption

Layer¹,

Ohe²,

Jj³

et al. 1997

Gastroenterology

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“…Highly purified porcine cholecystokinin-33 for intravenous infusion was purchased from Ferring (Malmo, Sweden). Synthetic human C C K 33 for radioimmunoassay was purchased from Peninsula Laboratories (St. Helens, UK); radioiodinated porcine PP ( 125I-PPP) from Novo Nordisk AS (Bagsvaerd, Denmark). MCT (Ceres-MCT-dietary oil) containing 56% octanoic acid (C 8) and 43% decanoic acid ( C 10), was from Bakker (Etten-Leur, The Netherlands).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men

Maas¹,

Hopman²,

Katan³

et al. 1996

Regulatory Peptides

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Long-chain triglycerides inhibit gastric acid secretion, but the effect of medium-chain triglycerides in humans is unknown. We compared the effects of intraduodenally perfused saline, medium-chain and long-chain triglycerides on gastrin-stimulated gastric acid secretion and cholecystokinin release. Eight healthy male volunteers participated in this study. Gastrin-stimulated gastric acid output was 9.4 ± 1.1 m m ol/30 min during saline perfusion. It was suppressed by medium-chain triglycerides by 43 ± 9% (P = 0.04 vs. saline) and by long-chain triglycerides by 74 ± 6% (P -0.0003 vs. saline). Thus medium-chain triglycerides inhibited gastrin-stimulated gastric acid secretion but less so than long-chain triglycerides. When compared to saline perfusion (73 ± 6 pM X 30 min) integrated plasma cholecystokinin concentrations were significantly elevated by long-chain triglycerides (96 ±5 pM X 30 min, P < 0,004) but not by medium-chain triglycerides perfusion (65 ± 7 pM X 30 min). We also investigated the role of cholecystokinin infusion on gastrin stimulated gastric acid secretion. Higher concentrations (191.4 ± 4,5 pM X 30 min) of CCK than released in the long-chain triglycerides perfusion experiment, did not suppress gastric acid secretion. Thus, circulating cholecystokinin appears not responsible for the inhibition of gastrin-stimulated gastric acid secretion by dietary fat.

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Role of cholecystokinin in the regulation of gastric emptying and pancreatic enzyme secretion in humans

Cited by 165 publications

References 23 publications

Therapy for Obesity Based on Gastrointestinal Hormones

Therapy for Obesity Based on Gastrointestinal Hormones

Altered postprandial motility in chronic pancreatitis: Role of malabsorption

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men

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