Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Konturek, Stanisław J.; Kwiecień, N; Obtulowicz, W; Kopp, B; Oleksy, J; Rovati, Lucio C.

doi:10.1159/000200218

Cited by 45 publications

(13 citation statements)

References 15 publications

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“…Though a consequent increase in antral motility and GE of solid food would be expected, it is possible that an increase in gastric acid, gastrin secretion and duodenogastric reflux could cause a reflex decrease in GE, through release of cholecystokinin and secretin 39. It would be invaluable to investigate the role of duodenogastric reflux in the pathogenesis of delayed GE in asthmatics.…”

Section: Discussionmentioning

confidence: 99%

Gastric Motility Following Ingestion of a Solid Meal in a Cohort of Adult Asthmatics

Amarasiri¹,

Pathmeswaran

Silva

et al. 2013

J Neurogastroenterol Motil

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Background/AimsAsthmatics have abnormal esophageal motility and increased prevalence of gastroesophageal reflux disease (GERD). The contribution of gastric motility is less studied. We studied gastric myoelectrical activity, gastric emptying (GE) and their association with GERD symptoms and vagal function in adult asthmatics.MethodsThirty mild, stable asthmatics and 30 healthy controls underwent real-time ultrasonography and 1 hour pre- and post-prandial cutaneous electrogastrography, following a test meal (480 kcal, 60% carbohydrate, 20% protein, 20% fat and 200 mL water). The percentage of normal slow waves and arrhythmias, dominant frequency and power, frequency of antral contractions, gastric emptying rate (GER) and antral motility index (MI) was calculated. Twenty-seven asthmatics underwent gastroscopy and in all subjects GERD symptoms were assessed by a validated questionnaire. Vagal function parameters were correlated with gastric motility parameters.ResultsThe asthmatics (37% male; 34.8 ± 8.4 years) and controls (50% male; 30.9 ± 7.7 years) were comparable. None had endoscopic gastric pathological changes. Twenty asthmatics described GERD symptoms. Twenty-two (73.3%) asthmatics showed a hypervagal response. Compared to controls, asthmatics had delayed GER and lower MI, lower percentage of normal gastric slow waves, more gastric dysrythmias and failed to increase the post-prandial dominant power. There was no correlation of GE and cutaneous electrogastrography parameters with presence of GERD symptoms or with vagal function.ConclusionsAsthmatics showed abnormal gastric myoelectrical activity, delayed GE and antral hypomotility in response to a solid meal compared to controls. There was no association with vagal function or GERD symptom status.

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Section: Discussionmentioning

confidence: 99%

Gastric Motility Following Ingestion of a Solid Meal in a Cohort of Adult Asthmatics

Amarasiri¹,

Pathmeswaran

Silva

et al. 2013

J Neurogastroenterol Motil

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“…CCK inhibits gastric emptying by relaxing the proximal part of the stomach and stimulating contraction of the pyloric sphincter (Chey et al 1970, Fisher et al 1973. CCK also inhibits gastric secretion in humans (Konturek et al 1990). In this study, hCG treatment of Ovx rats resulted in a fact that the inhibition of gastric emptying induced by hCG might be associated with CCK hypersecretion and that inhibition of gastric emptying caused by hypersecretion of hCG and CCK may explain the gastric distension and NVP seen in women during the first trimester of pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…Cholecystokinin (CCK), a 33 amino acid peptide extracted from porcine intestine (Jorpes & Mutt 1966), inhibits gastric emptying in animals (Debas et al 1975, Wu et al 2008 and humans (Konturek et al 1990) but has also been reported to stimulate colonic transit in vivo (Dinoso et al 1973, Harvey & Read 1973. The biological actions of CCK are mediated by two types of receptors, CCK 1 and CCK 2 (Noble et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Human chorionic gonadotropin regulates gastric emptying in ovariectomized rats

Seow¹,

Lee²,

Doong³

et al. 2012

Journal of Endocrinology

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Prolongation of gastrointestinal transit resulting in nausea and vomiting in pregnancy (NVP) is the most common phenomenon during the first trimester of pregnancy. Increased human chorionic gonadotropin (hCG) concentration during the first trimester is the most likely cause of NVP. The aim of this study was to investigate the effect of hCG on gastrointestinal transit and plasma concentrations of cholecystokinin (CCK) in ovariectomized (Ovx) rats. I.p. injection of hCG was used to evaluate the dose effect of hCG on gastrointestinal transit in Ovx rats. The CCK antagonist lorglumide was used to clarify the role of CCK in regulating gastrointestinal transit. Gastrointestinal transit was assessed 15 min after intragastric gavage of a mixture of 10% charcoal and Na 2 51 CrO 4 (0.5 mCi/ml). After i.p. administration of hCG, gastric emptying was inhibited in Ovx rats, but intestinal transit was not affected. Plasma CCK concentrations were increased in a dose-dependent manner after hCG treatment, and gastric emptying showed a significant negative correlation with CCK concentrations (PZ0.01, r 2 ZK0.5104). Peripheral administration (i.p.) of lorglumide, a selective CCK 1 receptor antagonist, attenuated the hCG-induced inhibition of gastric emptying in Ovx rats, whereas central administration via the i.c.v. route did not. hCG treatment of Ovx rats inhibits gastric emptying in a dose-dependent manner via a peripheral mechanism of CCK hypersecretion and activation of CCK 1 receptors. Journal of EndocrinologyResearch K-M SEOW, J-L LEE and others hCG and gastric emptying 216:3 307-314

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“…DU patients, as a group, tend to secrete more acid than normal subjects both at rest and in response to secretory stimulation (1) and this has been attributed mainly to hypergastrinemia and impaired inhibition of gastric functions partly by endogenous cholecystokinin (CCK) possibly due to the failure of this peptide to stimulate somatostatin release from antral D cells (2,3). CCK has been considered as a candidate of an enterogastrone (4), a hormonal substance released by fat in the intestine that causes not only physiological inhibition of gastric secretion (5) but also inhibits gastric emptying (6)(7)(8). Several animal and human studies (8,9) have shown that exogenous CCK as well as endogenous CCK released after feeding inhibits gastric emptying.…”

mentioning

confidence: 99%

“…CCK has been considered as a candidate of an enterogastrone (4), a hormonal substance released by fat in the intestine that causes not only physiological inhibition of gastric secretion (5) but also inhibits gastric emptying (6)(7)(8). Several animal and human studies (8,9) have shown that exogenous CCK as well as endogenous CCK released after feeding inhibits gastric emptying.…”

mentioning

confidence: 99%

Eradication ofHelicobacter pyloriRestores the Inhibitory Effect of Cholecystokinin on Gastric Motility in Duodenal Ulcer Patients

Konturek

2001

Scandinavian Journal of Gastroenterology

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SJ, Domschke W. Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on gastric motility in duodenal ulcer patients. Scand J Gastroenterol 2001;36:241-246.Background: Increased gastric emptying and defective action of endogenous cholecystokinin (CCK), that is known to inhibit this emptying, have been implicated in the pathogenesis of duodenal ulcer (DU). The aim of this double blind study was to assess whether CCK and somatostatin participate in the impairment of gastric motility in active DU patients before and after Helicobacter pylori eradication. Methods: Tests were undertaken in 10 DU patients without or with elimination of the action of endogenous CCK using loxiglumide, a selective CCK-A receptor antagonist, before and 4 weeks after eradication of H. pylori with 1 week triple therapy that resulted in healing of all DUs tested. The gastric emptying rate after feeding was determined using the 1 3 C-acetate breath test. Before each test, samples of gastric juice were obtained by aspiration using a nasogastric tube for determination of somatostatin using speci c radioimmunoassay. Results: Prior to H. pylori eradication gastric emptying half-time was 31 § 6 min in placebo-treated DU patients and this emptying rate was not signi cantly affected in tests after pretreatment with loxiglumide (10 mg/kg i.v.). Following eradication of H. pylori, in tests with placebo gastric emptying half-time was signi cantly longer (48 § 9 min) compared to that prior to H. pylori eradication. Pretreatment with loxiglumide in H. pylori eradicated DU patients signi cantly enhanced the gastric emptying rate with an emptying half-time of only 33 § 4 min. Eradication of H. pylori resulted in a signi cant increase in somatostatin concentration in gastric juice and loxiglumide signi cantly reduced this luminal somatostatin in H. pylori-eradicated subjects compared to values before anti-H. pylori therapy. Conclusions: 1) H. pylori infection in DU patients is accompanied by enhanced gastric emptying and reduction in luminal release of somatostatin; 2) the failure of loxiglumide to affect gastric emptying in H. pylori-infected DU patients might be attributed, at least in part, to the failure of endogenous CCK to control gastric motility due to de cient release of somatostatin; and 3) H. pylori-infected patients appear to exhibit a de cient somatostatin release by endogenous CCK that can be reversed by the eradication of H. pylori indicating that both CCK and somatostatin may contribute to normalization of gastric emptying following H. pylori eradication in DU patients.

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Cholecystokinin in the Inhibition of Gastric Secretion and Gastric Emptying in Humans

Cited by 45 publications

References 15 publications

Gastric Motility Following Ingestion of a Solid Meal in a Cohort of Adult Asthmatics

Gastric Motility Following Ingestion of a Solid Meal in a Cohort of Adult Asthmatics

Human chorionic gonadotropin regulates gastric emptying in ovariectomized rats

Eradication ofHelicobacter pyloriRestores the Inhibitory Effect of Cholecystokinin on Gastric Motility in Duodenal Ulcer Patients

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