Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Koop, Irmtraut; Ruppert-Seipp, Gabriele; Koop, H.; Schafmayer, A.; Arnold, R.

doi:10.1159/000200349

Cited by 26 publications

(6 citation statements)

References 16 publications

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“…This finding is in contrast with data from another study in humans30 in which an 81% increase in plasma CCK was observed after fundic distension. In contrast, antral distension does not appear to cause CCK secretion 30…”

Section: Discussioncontrasting

confidence: 99%

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia

Feinle¹,

Meier²,

Otto³

et al. 2001

Gut

176

145

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Background/aims-We aimed to evaluate the role of fat and cholecystokinin (CCK) in the pathophysiology of functional dyspepsia (FD) by investigating symptoms and plasma CCK levels following increasing doses of duodenal lipid during gastric distension, and the eVect of CCK-A receptor blockade. Subjects/methods-In study A, six FD patients were studied on three occasions during duodenal infusion of saline or lipid (1.1 (L-1) or 2 kcal/min (L-2)) and proximal gastric distensions. Six healthy subjects were also studied as controls during L-2 only. In study B, the eVect of the CCK-A antagonist dexloxiglumide (5 mg/ kg/h) on L-2 induced symptoms was studied in 12 FD patients. Changes in gastric volume at minimal distending pressure and plasma CCK (study A) were assessed, gastric distensions were performed using a barostat, and dyspeptic symptoms were monitored. Results-Lipid increased gastric volume compared with saline ( V (ml): saline 15 (20), L-1 122 (42), L-2 114 (28)) in patients and even more so in controls (221 (37); p<0.05). During distensions, symptoms were greater during L-2 than during saline or L-1, and greater in patients than in controls, while gastric compliance was smaller in patients than in controls (p<0.05). Lipid increased plasma CCK levels in patients and controls (p>0.05). Dexloxiglumide abolished the increase in gastric volume ( V (ml): dexloxiglumide 17 (9), placebo 186 (49)) and dyspeptic symptoms (sum of scores: dexloxiglumide 24 (7), placebo 44 (19)) during duodenal lipid infusion. Dexloxiglumide also reduced gastric compliance (ml/mm Hg: dexloxiglumide 51 (7), placebo 72 (11)) and symptoms (sum of scores: dexloxiglumide 101 (17), placebo 154 (21)) during gastric distension. Conclusion-CCK-A receptors are involved in the generation of dyspeptic symptoms by duodenal lipid during gastric distension. (Gut 2001;48:347-355)

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Section: Discussioncontrasting

confidence: 99%

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia

Feinle¹,

Meier²,

Otto³

et al. 2001

Gut

176

145

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“…This may suggest that, in contrast to PYY and ghrelin, gastric distension, enhanced by the greater amount of food eaten during the FAT-THL condition, may be a more important stimulus for PP. Indeed, moderate gastric distension with a balloon (volume: 600 ml) has been shown to cause a substantial (71%) increase in PP secretion in healthy volunteers (20). Alternatively, it is possible that the other macronutrients, carbohydrate and protein, are more important stimuli for PP secretion than fat.…”

Section: Discussionmentioning

confidence: 99%

Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid

Feinle‐Bisset

Patterson²,

Ghatei³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

140

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-Stimulation of cholecystokinin and glucagon-like peptide-1 secretion by fat is mediated by the products of fat digestion. Ghrelin, peptide YY (PYY), and pancreatic polypeptide (PP) appear to play an important role in appetite regulation, and their release is modulated by food ingestion, including fat. It is unknown whether fat digestion is a prerequisite for their suppression (ghrelin) or release (PYY, PP). Moreover, it is not known whether small intestinal exposure to fat is sufficient to suppress ghrelin secretion. Our study aimed to resolve these issues. Sixteen healthy young males received, on two separate occasions, 120-min intraduodenal infusions of a long-chain triglyceride emulsion (2.8 kcal/min) 1) without (condition FAT) or 2) with (FAT-THL) 120 mg of tetrahydrolipstatin (THL, lipase inhibitor), followed by a standard buffet-style meal. Blood samples for ghrelin, PYY, and PP were taken throughout. FAT infusion was associated with a marked, and progressive, suppression of plasma ghrelin from t ϭ 60 min (P Ͻ 0.001) and stimulation of PYY from t ϭ 30 min (P Ͻ 0.01). FAT infusion also stimulated plasma PP (P Յ 0.01), and the release was immediate. FAT-THL completely abolished the FAT-induced changes in ghrelin, PYY, and PP. In response to the meal, plasma ghrelin was further suppressed, and PYY and PP stimulated, during both FAT and FAT-THL infusions. In conclusion, in healthy humans, 1) the presence of fat in the small intestine suppresses ghrelin secretion, and 2) fat-induced suppression of ghrelin and stimulation of PYY and PP is dependent on fat digestion. lipase inhibition; gut hormone secretion A NUMBER OF GASTROINTESTINAL PEPTIDES play a role in the regulation of energy intake in humans, including cholecystokinin (CCK) (19, 27), glucagon-like peptide-1 (GLP-1) (13, 17), peptide YY (PYY) (4), pancreatic polypeptide (PP) (5), and ghrelin (42). The secretion of CCK, GLP-1, and PYY from intestinal cells, and PP from the pancreas, is stimulated by meal ingestion or infusion of nutrients into the small intestine (10,18,21,29). In contrast, ghrelin is secreted by the stomach, and plasma concentrations increase during fasting and are suppressed by a meal (7,8).Plasma ghrelin concentrations decrease rapidly following food ingestion, and there is evidence that ghrelin plays a role in meal initiation (7,8). Intravenously administered ghrelin has been shown to stimulate appetite and increase food intake in humans (42). Both carbohydrate and fat, when ingested orally, suppress ghrelin secretion (9, 15), whereas protein may stimulate ghrelin secretion (9) or have no effect (15). Although until recently it has been unclear whether the suppressive effect of carbohydrate and fat on ghrelin secretion is mediated by the presence of nutrients in the stomach, the small intestine, and/or the circulation, recent animal (41) and human (30) studies indicate that the interaction of nutrients with the small intestine is important in the glucose-induced modulation of ghrelin secretion. In rats, the prevention of gastric empty...

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“…In addition, we perfused the peptone through the stomach, with continuous aspiration of the antrum to avoid any effects of distension on gastrin release. Koop et al [12] have demonstrated that fundic distension in man increases basal gastrin by 31 %. which may explain why our peptone-stimulated gastrin release was rela tively small compared with previous studies of intragastric titration [17,29], In addition to distending the stomach, the method of intragastric titration may also chemically stimulate gastrin cells to a greater extent since the peptone is not perfused through the stomach as it was in our study, but is rela tively static.…”

Section: Discussionmentioning

confidence: 97%

“…To test this, we measured plasma gastrin concentrations during stimula tion of the stomach with 4% peptone solu tions at pH 2.5 and at pH 5.5 before and after suppression of H. pylori. The gastric pH was kept constant by titration with alkali, and the meal was perfused through the stomach by a method that we have previously used to avoid the effects of gastric distension [10][11][12],…”

mentioning

confidence: 99%

pH-Dependent Secretion of Gastrin in Duodenal Ulcer Disease: Effect of Suppressing <i>Helicobacter pylori</i>

Moss

Ayesu²,

Li³

et al. 1992

Digestion

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Patients with duodenal ulcers and Helicobacter pylori infection have elevated plasma gastrin concentrations which fall after suppression of the organism. This may be due to H. pylori elevating the pH of the antral mucous layer, therefore preventing luminal acid from inhibiting gastrin release. To test this idea, we measured the plasma gastrin concentrations under basal conditions and in response to 4% peptone when the gastric lumen was maintained at pH 2.5 and at pH 5.5 by gastric perfusion. We studied 11 duodenal ulcer patients before and after suppression of H. pylori. Gastrin concentrations were significantly higher before suppression of H. pylori than after treatment in all three states; basal gastrin (pmol/l) fell from 9.2 (3.7-23, median and range) to 5.1 (1.7-15) after treatment; from 11.3 (3.8-29) to 5.9 (5.7-6.1) at pH 2.5 and from 15.2 (3.9-32) to 7.15 (6.1-14) at pH 5.5. The ratio of peptone-stimulated gastrin at pH2.5/pH5.5 was similar before (0.8; 0.5-1.7) and after (0.8; 0.5-1.1) suppression of H. pylori. These results indicate that infection with H. pylori increases basal and peptone-stimulated plasma gastrin concentrations, and that this response is independent of luminal pH.

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Cholecystokinin Release by Gastric Distension – An Atropine-Sensitive Mechanism

Cited by 26 publications

References 16 publications

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia

Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid

pH-Dependent Secretion of Gastrin in Duodenal Ulcer Disease: Effect of Suppressing <i>Helicobacter pylori</i>

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