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Van Erpecum - One of the best experts on this subject based on the ideXlab platform.
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acute intraduodenal bile salt depletion leads to strong Gallbladder Contraction altered antroduodenal motility and high plasma motilin levels in humans
Neurogastroenterology and Motility, 2000Co-Authors: Van Bergehenegouwen, Van Solinge, Van ErpecumAbstract:Cholecystokinin is the main hormone involved in postprandial Gallbladder Contraction. There is also considerable Gallbladder Contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting Gallbladder Contraction. We wanted to elucidate whether a similar control mechanism on Gallbladder Contraction exists in the fasting state. We therefore performed Gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day–1) oral cholestyramine. Acute cholestyramine strongly decreased Gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between Gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P < 0.03) with markedly longer phase II (P < 0.005). Fasting Gallbladder volumes 24 h later were still strongly decreased but gradually increased to pretreatment levels. Before and after 8 days cholestyramine, interdigestive and postprandial Gallbladder emptying, intestinal migrating motor complex and hormone levels did not differ. We conclude that acute (but not chronic) intraduodenal bile salt depletion with cholestyramine affects Gallbladder and antroduodenal motility, possibly partly related to motilin release.
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Acute intraduodenal bile salt depletion leads to strong Gallbladder Contraction, altered antroduodenal motility and high plasma motilin levels in humans.
Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2000Co-Authors: Portincasa, Peeters, Van Berge-henegouwen, Van Solinge, Palasciano, Van ErpecumAbstract:Cholecystokinin is the main hormone involved in postprandial Gallbladder Contraction. There is also considerable Gallbladder Contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting Gallbladder Contraction. We wanted to elucidate whether a similar control mechanism on Gallbladder Contraction exists in the fasting state. We therefore performed Gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day–1) oral cholestyramine. Acute cholestyramine strongly decreased Gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between Gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P
P. Hildebrand - One of the best experts on this subject based on the ideXlab platform.
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duodenal phytohaemagglutinin red kidney bean lectin stimulates Gallbladder Contraction in humans
Acta Physiologica, 2008Co-Authors: A K Purhonen, Karlheinz Herzig, Hansjoachim Gabius, Sabine Andre, S Ketterer, D Matzinger, C Beglinger, P. HildebrandAbstract:Aim: Lectins, carbohydrate-specific proteins without enzymatic activity on the ligand, are daily ingested plant proteins which survive the passage through the gastrointestinal tract in a biologically active form. Their binding to glycan determinants of natural glycoconjugates can trigger biological effects. The lectin phytohaemagglutinin (PHA) is abundantly present in red kidney beans and induces cholecystokinin (CCK) release in rats. The aim of the study was to investigate the effect of intraduodenal administration of PHA on plasma CCK levels and Gallbladder Contraction in humans and to elucidate potential mechanisms of action. Methods: Five healthy volunteers underwent four studies. After a basal intraduodenal saline infusion for 30 min, PHA or heat-inactivated PHA was infused in increasing doses: 150 μg, 1.5 mg and 15 mg for 30 min each. Intravenous saline, CCK1 receptor antagonist dexloxiglumide or atropine were administered in random order. Gallbladder volumes were measured by ultrasonography and plasma CCK levels by radioimmunoassay. Results: Intraduodenal PHA induced Gallbladder Contraction in a dose-dependent fashion starting with the lowest dose. The highest dose reduced the Gallbladder volume to 65.3 ± 9.4% of basal volume (P < 0.001) whereas heat-inactivated PHA did not have any effect. Blocking CCK1 or muscarinic receptors completely abolished PHA-stimulated Gallbladder Contraction (dexloxiglumide 208.7 ± 23.7%; atropine 104 ± 7.0% of basal volume) while none of the treatments affected CCK levels. Conclusion: Duodenal administration of PHA potently stimulates Gallbladder Contraction in humans. This Contraction is mediated via cholinergic pathway.
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Duodenal phytohaemagglutinin (red kidney bean lectin) stimulates Gallbladder Contraction in humans.
Acta physiologica (Oxford England), 2008Co-Authors: A K Purhonen, Christoph Beglinger, Karlheinz Herzig, Hansjoachim Gabius, Sabine Andre, S Ketterer, D Matzinger, P. HildebrandAbstract:Aim: Lectins, carbohydrate-specific proteins without enzymatic activity on the ligand, are daily ingested plant proteins which survive the passage through the gastrointestinal tract in a biologically active form. Their binding to glycan determinants of natural glycoconjugates can trigger biological effects. The lectin phytohaemagglutinin (PHA) is abundantly present in red kidney beans and induces cholecystokinin (CCK) release in rats. The aim of the study was to investigate the effect of intraduodenal administration of PHA on plasma CCK levels and Gallbladder Contraction in humans and to elucidate potential mechanisms of action. Methods: Five healthy volunteers underwent four studies. After a basal intraduodenal saline infusion for 30 min, PHA or heat-inactivated PHA was infused in increasing doses: 150 μg, 1.5 mg and 15 mg for 30 min each. Intravenous saline, CCK1 receptor antagonist dexloxiglumide or atropine were administered in random order. Gallbladder volumes were measured by ultrasonography and plasma CCK levels by radioimmunoassay. Results: Intraduodenal PHA induced Gallbladder Contraction in a dose-dependent fashion starting with the lowest dose. The highest dose reduced the Gallbladder volume to 65.3 ± 9.4% of basal volume (P
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Postprandial control of Gallbladder Contraction and exocrine pancreatic secretion in man
European journal of clinical investigation, 1992Co-Authors: Christoph Beglinger, P. Hildebrand, G. Adler, Baseli Werth, H. Luo, Fabiola Delco, K. GyrAbstract:. To explore the interactions between chole-cystokinin (CCK) and the cholinergic system, we compared the effect of cholinergic or peptidergic CCK blockade on Gallbladder Contraction and pancreatic enzyme secretion using atropine and loxiglumide (a specific CCK antagonist) as pharmacological tools. Gallbladder Contraction was measured by sonography and pancreatic secretion by a marker perfusion and aspiration technique. Graded doses of exogenous CCK8 induced dose-dependent Contractions of the Gallbladder and increasing enzyme outputs. Loxiglumide (10 mg kg-1 h-1) abolished the Gallbladder response and prevented an increase in pancreatic enzyme secretion to CCK8. Atropine (5 μg kg-1 h-1), however, only reduced Gallbladder Contraction and enzyme output to CCK8. Gallbladder volumes decreased maximally to 12±4% after oral food, whereas enzyme output and plasma CCK levels increased 6- to 8-fold. Loxiglumide completely abolished Gallbladder Contraction and inhibited enzyme secretion by 30%. Atropine caused a small reduction in Gallbladder volumes, but essentially blocked postprandial enzyme secretion. The results indicate that CCK is the major regulator of Gallbladder Contraction with the cholinergic system modulating the response, while the exocrine pancreas is crucially dependent on a cholinergic background with CCK modulating the secretory response.
Christoph Beglinger - One of the best experts on this subject based on the ideXlab platform.
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Duodenal phytohaemagglutinin (red kidney bean lectin) stimulates Gallbladder Contraction in humans.
Acta physiologica (Oxford England), 2008Co-Authors: A K Purhonen, Christoph Beglinger, Karlheinz Herzig, Hansjoachim Gabius, Sabine Andre, S Ketterer, D Matzinger, P. HildebrandAbstract:Aim: Lectins, carbohydrate-specific proteins without enzymatic activity on the ligand, are daily ingested plant proteins which survive the passage through the gastrointestinal tract in a biologically active form. Their binding to glycan determinants of natural glycoconjugates can trigger biological effects. The lectin phytohaemagglutinin (PHA) is abundantly present in red kidney beans and induces cholecystokinin (CCK) release in rats. The aim of the study was to investigate the effect of intraduodenal administration of PHA on plasma CCK levels and Gallbladder Contraction in humans and to elucidate potential mechanisms of action. Methods: Five healthy volunteers underwent four studies. After a basal intraduodenal saline infusion for 30 min, PHA or heat-inactivated PHA was infused in increasing doses: 150 μg, 1.5 mg and 15 mg for 30 min each. Intravenous saline, CCK1 receptor antagonist dexloxiglumide or atropine were administered in random order. Gallbladder volumes were measured by ultrasonography and plasma CCK levels by radioimmunoassay. Results: Intraduodenal PHA induced Gallbladder Contraction in a dose-dependent fashion starting with the lowest dose. The highest dose reduced the Gallbladder volume to 65.3 ± 9.4% of basal volume (P
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role of free fatty acids in regulating gastric emptying and Gallbladder Contraction
Digestion, 2006Co-Authors: Lukas Degen, Daniel Matzinger, Juergen Drewe, Sonja Nissle, Helmut Maecke, Hans Lengsfeld, Paul Hadvary, Christoph BeglingerAbstract:The limited effectiveness of orlistat, an inhibitor of gastrointestinal lipases, in inhibiting fat digestion is not completely understood. Therefore we studied the effect of orally and duodenally administered orlistat on gastric emptying, cholecystokinin (CCK) secretion, and Gallbladder Contraction. In healthy males, gastric emptying of solids and fat were quantified scintigraphically, Gallbladder Contraction by ultrasound and CCK release by radioimmunoassay. Three studies were performed: (1) oral and (2) duodenal orlistat with a fat-containing meal, and (3) duodenal orlistat with a fat-free meal. Gastric emptying rates of solids and fat (T50% accelerated by 16 and by 22%, p < 0.05, respectively) were significantly faster after duodenal perfusion of orlistat; Gallbladder Contraction and CCK release were reduced under these conditions (p < 0.005, respectively). With oral orlistat no significant effect was documented on these parameters. We conclude that fat hydrolysis is essential in the regulation of fat-induced gastric emptying and Gallbladder Contraction.
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blockade of grp receptors inhibits gastric emptying and Gallbladder Contraction but accelerates small intestinal transit
Gastroenterology, 2001Co-Authors: Lukas Degen, Christoph Beglinger, Fuping Peng, Annette Collet, Livid Rossi, Silvia Ketterer, Yolanda Serrano, Finn Larsen, Pius HildebrandAbstract:Abstract Background & Aims: This study was designed to characterize [D-F 5 Phe 6 D-Ala 11 ]Bn(6-13)OMe (BIM26226) as a gastrin-releasing peptide (GRP)-preferring bombesin receptor antagonist and to determine whether GRP physiologically regulates gastrointestinal motility. Intravenous BIM26226 (5–500 μg · kg −1 · h −1 ) inhibits GRP-induced Gallbladder Contraction and plasma cholecystokinin (CCK) release in a dose-dependent fashion. Methods: Gastric emptying and small bowel transit of a solid meal were quantified using scintigraphy. Meal-stimulated Gallbladder Contraction was measured by sonography in a 2-period crossover design. Results: Intravenous BIM26226 potently inhibited gastric lag time (114 ± 7 vs. 41 ± 6 minutes [control]) and gastric emptying rate (0.11 ± 0.02%/min vs. 0.26 ± 0.04%/min [control]), whereas concomitant infusion of BIM26226 accelerated small bowel transit time (153 ± 41 vs. 262 ± 20 minutes [control]). A continuous liquid meal perfusion into the duodenum induced complete Gallbladder Contraction (t 50% , 35 ± 4 minutes), which BIM26226 inhibited significantly (t 50% , 64 ± 8 minutes). BIM26226 did not alter plasma CCK response, indicating that circulating CCK did not mediate these effects. Conclusions: These data show that BIM26226 is a potent antagonist of exogenous and endogenous GRP and suggest that GRP is a major physiologic regulator of gastric emptying, small bowel transit, and Gallbladder Contraction. GASTROENTEROLOGY 2001;120:361-368
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Postprandial control of Gallbladder Contraction and exocrine pancreatic secretion in man
European journal of clinical investigation, 1992Co-Authors: Christoph Beglinger, P. Hildebrand, G. Adler, Baseli Werth, H. Luo, Fabiola Delco, K. GyrAbstract:. To explore the interactions between chole-cystokinin (CCK) and the cholinergic system, we compared the effect of cholinergic or peptidergic CCK blockade on Gallbladder Contraction and pancreatic enzyme secretion using atropine and loxiglumide (a specific CCK antagonist) as pharmacological tools. Gallbladder Contraction was measured by sonography and pancreatic secretion by a marker perfusion and aspiration technique. Graded doses of exogenous CCK8 induced dose-dependent Contractions of the Gallbladder and increasing enzyme outputs. Loxiglumide (10 mg kg-1 h-1) abolished the Gallbladder response and prevented an increase in pancreatic enzyme secretion to CCK8. Atropine (5 μg kg-1 h-1), however, only reduced Gallbladder Contraction and enzyme output to CCK8. Gallbladder volumes decreased maximally to 12±4% after oral food, whereas enzyme output and plasma CCK levels increased 6- to 8-fold. Loxiglumide completely abolished Gallbladder Contraction and inhibited enzyme secretion by 30%. Atropine caused a small reduction in Gallbladder volumes, but essentially blocked postprandial enzyme secretion. The results indicate that CCK is the major regulator of Gallbladder Contraction with the cholinergic system modulating the response, while the exocrine pancreas is crucially dependent on a cholinergic background with CCK modulating the secretory response.
Dal Mo Yang - One of the best experts on this subject based on the ideXlab platform.
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Gallbladder Contraction at CT and sonography secondary to bowel preparation for colonoscopy
Abdominal Radiology, 2020Co-Authors: Yeji Shin, Sang Won Kim, Hyun Cheol Kim, Seong Jin Park, Dal Mo YangAbstract:Purpose To investigate volume changes of the Gallbladder at computed tomography (CT) following bowel preparation for colonoscopy and to evaluate the incidence of Gallbladder Contraction at abdominal sonography performed with colonoscopy on the same day. Methods During a 1-year period, 222 patients underwent abdominal CT (CT_1) and colonoscopy on the same day. Among them, 123 patients had prior CT imaging without receiving colonoscopy in the past were enrolled. Manual estimates of 3D Gallbladder volume were obtained from two CT scans to evaluate whether Gallbladder volume changed as a result of bowel preparation for colonoscopy. During the same 1-year period, another 89 patients underwent abdominal sonography and colonoscopy on the same day (sonography group). The short-axis diameters of the Gallbladder on the longitudinal scan of sonography from these patients were obtained. Results Gallbladder volume was significantly larger on prior CT without colonoscopy (31.7 ± 15.4 cm^3) than on CT_1 (20.3 ± 11.1 cm^3) ( p
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Gallbladder Contraction at ct and sonography secondary to bowel preparation for colonoscopy
Abdominal Radiology, 2020Co-Authors: Yeji Shin, Sang Won Kim, Hyun Cheol Kim, Seong Jin Park, Dal Mo YangAbstract:PURPOSE To investigate volume changes of the Gallbladder at computed tomography (CT) following bowel preparation for colonoscopy and to evaluate the incidence of Gallbladder Contraction at abdominal sonography performed with colonoscopy on the same day. METHODS During a 1-year period, 222 patients underwent abdominal CT (CT1) and colonoscopy on the same day. Among them, 123 patients had prior CT imaging without receiving colonoscopy in the past were enrolled. Manual estimates of 3D Gallbladder volume were obtained from two CT scans to evaluate whether Gallbladder volume changed as a result of bowel preparation for colonoscopy. During the same 1-year period, another 89 patients underwent abdominal sonography and colonoscopy on the same day (sonography group). The short-axis diameters of the Gallbladder on the longitudinal scan of sonography from these patients were obtained. RESULTS Gallbladder volume was significantly larger on prior CT without colonoscopy (31.7 ± 15.4 cm3) than on CT1 (20.3 ± 11.1 cm3) (p < 0.001). Gallbladder volume decreased by more than 50% in 41 of 123 patients (33%) who underwent abdominal CT and colonoscopy on the same day, compared with standard CT. In the sonography group (n = 89), the short-axis diameters of the Gallbladder were less than 1.5 cm in 41 patients (46%) and less than 1.0 cm in 17 patients (19%). CONCLUSION Contracted Gallbladder secondary to bowel preparation can be seen on imaging when performed with same-day colonoscopy. Such a situation may lead to the incomplete or inadequate evaluation of the Gallbladder on imaging with same-day colonoscopy.
Van Bergehenegouwen - One of the best experts on this subject based on the ideXlab platform.
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acute intraduodenal bile salt depletion leads to strong Gallbladder Contraction altered antroduodenal motility and high plasma motilin levels in humans
Neurogastroenterology and Motility, 2000Co-Authors: Van Bergehenegouwen, Van Solinge, Van ErpecumAbstract:Cholecystokinin is the main hormone involved in postprandial Gallbladder Contraction. There is also considerable Gallbladder Contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting Gallbladder Contraction. We wanted to elucidate whether a similar control mechanism on Gallbladder Contraction exists in the fasting state. We therefore performed Gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day–1) oral cholestyramine. Acute cholestyramine strongly decreased Gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between Gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P < 0.03) with markedly longer phase II (P < 0.005). Fasting Gallbladder volumes 24 h later were still strongly decreased but gradually increased to pretreatment levels. Before and after 8 days cholestyramine, interdigestive and postprandial Gallbladder emptying, intestinal migrating motor complex and hormone levels did not differ. We conclude that acute (but not chronic) intraduodenal bile salt depletion with cholestyramine affects Gallbladder and antroduodenal motility, possibly partly related to motilin release.
