Gallbladder Emptying In Patients Research Articles

Single-Dose Metformin Enhances Bile Acid-Induced Glucagon-Like Peptide-1 Secretion in Patients With Type 2 Diabetes.

Despite a position as the first-line pharmacotherapy in type 2 diabetes, the glucose-lowering mechanisms of metformin remain to be fully clarified. Gut-derived modes of action, including suppression of bile acid reabsorption and a resulting increase in glucagon-like peptide-1 (GLP-1) secretion, have been proposed. The aim of this study was to assess the GLP-1 secretory and glucometabolic effects of endogenously released bile, with and without concomitant single-dose administration of metformin in patients with type 2 diabetes. Randomized, placebo-controlled, and double-blinded crossover study. This study was conducted at Center for Diabetes Research, Gentofte Hospital, Denmark. Fifteen metformin-treated patients with type 2 diabetes; all participants completed the study. Four experimental study days in randomized order with administration of either 1500 mg metformin or placebo in combination with intravenous infusion of cholecystokinin (0.4 pmol × kg-1 × min-1) or saline. Plasma GLP-1 excursions as measured by baseline-subtracted area under the curve. Single-dose metformin further enhanced bile acid-mediated induction of GLP-1 secretion (P = 0.02), whereas metformin alone did not increase plasma GLP-1 concentrations compared with placebo (P = 0.17). Metformin, both with (P = 0.02) and without (P = 0.02) concomitant cholecystokinin-induced gallbladder emptying, elicited reduced plasma glucose excursions compared with placebo. No GLP-1-mediated induction of insulin secretion or suppression of glucagon was observed. Metformin elicited an enhancement of the GLP-1 response to cholecystokinin-induced gallbladder emptying in patients with type 2 diabetes, whereas no derived effects on insulin or glucagon secretion were evident in this acute setting.

Postprandial gallbladder emptying in patients with type 2 diabetes: potential implications for bile-induced secretion of glucagon-like peptide 1.

Recent preclinical work has suggested that postprandial flow of bile acids into the small intestine potentiates nutrient-induced glucagon-like peptide 1 (GLP1(GCG)) secretion via bile acid-induced activation of the G protein-coupled receptor TGR5 in intestinal L cells. The notion of bile-induced GLP1 secretion combined with the findings of reduced postprandial gallbladder emptying in patients with type 2 diabetes (T2DM) led us to speculate whether reduced postprandial GLP1 responses in some patients with T2DM arise as a consequence of diabetic gallbladder dysmotility. In a randomised design, 15 patients with long-standing T2DM and 15 healthy age-, gender- and BMI-matched control subjects were studied during 75-g oral glucose tolerance test (OGTT) and three isocaloric (500 kcal) and isovolaemic (350 ml) liquid meals: i) 2.5 g fat, 107 g carbohydrate and 13 g protein; ii) 10 g fat, 93 g carbohydrate and 11 g protein; and iii) 40 g fat, 32 g carbohydrate and 3 g protein. Basal and postprandial plasma concentrations of glucose, insulin, C-peptide, glucagon, GLP1, glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin and gastrin were measured. Furthermore, gallbladder emptying and gastric emptying were examined. Gallbladder emptying increased with increasing meal fat content, but no intergroup differences were demonstrated. GIP and GLP1 responses were comparable among the groups with GIP levels being higher following high-fat meals, whereas GLP1 secretion was similar after both OGTT and meals. In conclusion, patients with T2DM exhibited normal gallbladder emptying to meals with a wide range of fat content. Incretin responses were similar to that in controls, and an association with postprandial gallbladder contraction could not be demonstrated.

Gallbladder Kinetics: Correlation between Gall Bladder Emptying in Patients With and Without Cholelithiasis by Ultrasonography

Background: Gallstone disease or cholelithiasis, is one of the most common surgical problems worldwide. The assessment of gallbladder kinetics in patients with cholelithiasis as well as in patients with high risk for cholelithiasis could play a significant role in better management and is recommended as a routine workup of biliary system in these patients.Objectives: This study was carried out to establish the relationship between impaired gall bladder emptying and gall bladder stones. It also aimed at finding out correlation between chosen risk factors. Materials and Methods: Eighty six subjects with cholelithiasis and 35 controls (without cholelithiasis) were studied. Pre-prandial gall bladder volume was measured after 6 hours of fasting, gallbladder emptying was stimulated by fatty meals of 610 and 740Kcal and post-prandial gallbladder volume was measured after a period of two hours with ultrasound. The difference of pre-prandial and postprandial gall bladder volume was calculated. Results: Gallbladder emptying was significantly more (p < 0.001) in the control group than in the group of subjects with cholelithiasis. In the case group the mean difference of volume was 9.2±7.1 cc. While in control group the mean difference of volume was 17.6±14.3. The prevalence of cholelithiasis was significantly high in females between 26- 35 years of age group and in patients with nonalcoholic fatty liver disease and in patients who had first degree relative with gall stone. Incidence of silent gall stone was also statistically significant. Conclusion: Impaired gallbladder emptying was found to be strongly associated with gall stones. NJR I VOL 2 I ISSUE 1 13-17 Jan-June, 2012 DOI: http://dx.doi.org/10.3126/njr.v2i1.6973

Gallbladder Emptying in Patients with Major Depression: A Case Series

Although several adverse effects of antidepressants on the gastrointestinal tract have been described (bleeding, constipation, dolichocolon), their influence on gallbladder motility was not investigated.The aim of our study was to investigate the effects of selected antidepressants on gallbladder emptying in patients with major depression. The study was set up as an open clinical trial, with the same intervention (ingestion of test meal provoking gallbladder emptying) undertaken in 112 patients with major depression. There were 30 patients not taking antidepressants (the control group), 25 patients taking amitriptyline, 30 patients taking maprotiline, and 27 patients taking fluoxetine. The volume of gallbladder in the study patients was measured by ultrasonography before the test meal, and 15, 30, 45 and 60 min after the meal. 1 h after ingestion of the study meal, the amitriptyline group showed incomplete gallbladder emptying (F=10.829, df=3, p=0.000; mean residual volume 11.0±6.1 mL), while in the control, maprotiline and fluoxetine groups emptying of gallbladder was complete (mean residual volumes 5.0±3.3 mL, 5.6±3.7 mL and 5.7±2.3 mL, respectively). In patients with cholecystitis, it would be wise to use antidepressants which do not impair gallbladder emptying, like maprotiline or fluoxetine, and to avoid amitriptyline.

Gallbladder emptying in patients with primary sclerosing cholangitis

To assess gallbladder emptying and its association with cholecystitis and abdominal pain in patients with primary sclerosing cholangitis (PSC). Twenty patients with PSC and ten healthy subjects were investigated. Gallbladder fasting volume, ejection fraction and residual volume after ingestion of a test meal were compared in patients with PSC and healthy controls using magnetic resonance imaging. Symptoms, thickness and contrast enhancement of the gallbladder wall and the presence of cystic duct strictures were also assessed. Median fasting gallbladder volume in patients with PSC [67 (19-348) mL] was twice that in healthy controls [32 (16-55) mL] (P < 0.05). The median postprandial gallbladder volume in patients with PSC was significantly larger than that in healthy controls (P < 0.05). There was no difference in ejection fraction, gallbladder emptying volume or mean thickness of the gallbladder wall between PSC patients and controls. Contrast enhancement of the gallbladder wall in PSC patients was higher than that in controls; (69% +/- 32%) and (42% +/- 21%) (P < 0.05). No significant association was found between the gallbladder volumes and occurrence of abdominal pain in patients and controls. Patients with PSC have increased fasting gallbladder volume. Gallbladder Mucosal dysfunction secondary to chronic cholecystitis, may be a possible mechanism for increased gallbladder.

Ultrasonographic evaluation of gallbladder dysfunction in patients with functional dyspepsia

The study aims to observe the gallbladder emptying in patients with functional dyspepsia, by means of ultrasonographic method described by Dodd et al. We measured the corelation between symptoms and presence of gallbladder dysfunction after a solid meal. Study also aims to evaluate the influence of Helicobacter pylori infection on gallbladder motility. Gallbladder and gastric evacuation were analized for identiffication of coordination problems between gastric and biliary motility.

15 Decreased Postprandial Gallbladder Emptying in Patients with Black Pigment Stones: A Comparative Study in Patients with Cholesterol Stones and Normal Subjects

15 Decreased Postprandial Gallbladder Emptying in Patients with Black Pigment Stones: A Comparative Study in Patients with Cholesterol Stones and Normal Subjects

Decreased postprandial gallbladder emptying in patients with black pigment stones

To analyze gallbladder contractility in patients with black pigment stones (BPSs) and to compare this with patients with cholesterol stones (CSs) and healthy volunteers. The pattern of bile evacuation from the gallbladder was quantified by computer cholescintigraphy in 28 normal subjects, 22 patients with CSs and 14 with BPSs. The parameters of gallbladder contractility included ejection period (EP), ejection fraction (EF) and ejection rate (ER). A significantly shorter EP was observed in patients with BPSs in comparison to those with CSs (t = 2.4, P < 0.05). EF in BPS patients significantly decreased in comparison to that in CS and normal subjects (t = 6.4, P < 0.0001; t = 2.1, P < 0.05). EF in CS patients also significantly decreased in comparison to that in normal subjects (t = -3.0, P < 0.005). Consequently, ER in patients with BPSs and CSs was significantly smaller than that in normal subjects (t = 3.1, P < 0.005; t = -3.5, P < 0.001). Moreover, in cases where postprandial reflux of a radioisotope into the common hepatic duct from the gallbladder was observed, EF and ER of either CS or BPS patients showed a significant reduction. Bile evacuation from the gallbladder is reduced in patients with BPSs, in comparison to those with CSs and to healthy volunteers. Bile stagnation due to impaired gallbladder kinetics seems to be one of the predisposing factors for the development of BPSs.

Prokinetic effect of ??-adrenergic antagonist, and ??-adrenergic antagonist on gall-bladder motility in humans with gall-stone disease

The effects of cholinergic agents and vagal control on gall-bladder motility are well defined. Alpha adrenergic antagonists have been found in previous studies to have a prokinetic effect on gall-bladder motility in normal human patients. Their effects have not, however, been fully elucidated in patients with gall-stone disease. Our aim was to determine the effects of alpha-antagonists and beta-antagonists on gall-bladder motility in human patients with gall-stone disease. In this single-blind, three-way crossover study, a slow release formulation of 80 mg propranolol (beta-antagonist), and 25 mg indoramin (alpha-antagonist), and placebo were administered separately to 10 patients with gall-stone disease on three separate days 8 h before assessment of gall-bladder volumes by ultrasonography. Gall-bladder volumes were assessed in the fasting state and at 5 min intervals for 50 min after a standard proprietary enteral feed (Ensure 180 ml, Abbott). Differences between the placebo and postadrenergic antagonist scan volumes were tested using the Wilcoxon-signed rank test. There were no significant differences in the mean fasting gall-bladder volumes after receiving propranolol, indoramin and placebo (23.6+/-3.9, 22.3+/-4.3, 26.8+/-7.2 ml, mean+/-SEM, respectively). In the postprandial period, however, indoramin significantly enhanced postprandial gall-bladder emptying compared with placebo between 5 and 30 min (P<0.05) after which refilling commenced. There were no significant postprandial gall-bladder volume differences between propranolol and placebo. Indoramin, an alpha-adrenergic antagonist, acts as a prokinetic agent enhancing postprandial gall-bladder emptying in patients with gall-stone disease. This effect is similar to its effect on postprandial gall-bladder emptying in healthy individuals.

Gall Bladder Emptying in Patients with Corrosive-Induced Esophageal Strictures

Ingestion of corrosive substances can lead to strictures of the esophagus and stomach. Cicatrization of the lower part of the esophagus can entrap vagal fibers in the process of fibrosis. The aim of the present study was to evaluate gallbladder dysfunction as a sequel to vagal damage in patients with corrosive-induced esophageal strictures. The cephalic phase of gallbladder emptying was stimulated by modified sham feeding according to the chew-and-spit method. Gallbladder volume was measured by ultrasonography using the ellipsoid method after an overnight fast and every 15 min for a period of 90 min after sham feeding in 22 patients and 10 controls. Mean fasting gallbladder volume was significantly greater in patients than in controls (22.09 +/- 9.78 vs. 14.61 +/- 4.42 ml; P = 0.025). After sham feeding the gallbladder ejection fraction was significantly lower in patients than in controls (32.86 +/- 17.21 vs. 49.40 +/- 7.86%; P = 0.007). Patients with cicatrization in the distal one-third of the esophagus had a greater basal gallbladder volume (24.57 +/- 9.2 ml) and significantly lower ejection fraction (20.47 +/- 8.9%) than patients with strictures at other sites (gallbladder volume, 18.50 +/- 10.69 ml; ejection fraction, 47.48 +/- 13.3%; P = 0.001). In conclusion, patients with corrosive-induced esophageal strictures, especially those in the distal one-third, had an increased fasting gallbladder volume and decreased cephalic phase of gallbladder emptying, pointing to impaired vagal cholinergic transmission, possibly due to vagal entrapment in the cicatrization process.

The hunt for microlithiasis in idiopathic acute recurrent pancreatitis: Should we abandon the search or intensify our efforts?

The hunt for microlithiasis in idiopathic acute recurrent pancreatitis: Should we abandon the search or intensify our efforts?

Cisapride improves gallbladder emptying in patients with type 2 diabetes mellitus.

Gallbladder motor function is impaired in many patients with diabetes, and may be related to cholinergic nerve damage. Cisapride is a prokinetic drug of the gastrointestinal tract and acts by releasing acetylcholine from cholinergic nerve endings. The aim of this study was to determine the effect of cisapride on gallbladder emptying in patients with type 2 diabetes mellitus (DM). Gallbladder emptying and tests for autonomic neuropathy (AN) were performed in 27 patients with type 2 DM and in 10 healthy subjects. Gallbladder emptying was studied by using real-time ultrasonography after an overnight fast, and after the subjects received a breakfast that contained 2500 J. Gallbladder emptying was repeated after the treatment with cisapride (10 mg t.i.d.) for 1 week in all subjects. Abnormal gallbladder emptying was present in 14 (51.9%) patients. The residual gallbladder volume (mean +/- SEM) was higher (9.3 +/- 1.0 vs 4.6 +/- 0.6; P = 0.002), and ejection fraction was lower (57.4 +/- 4.0 vs 74.2 +/- 2.4; P = 0.015) in diabetic patients than it was in healthy subjects. Cisapride produced a reduction in fasting and residual volumes (24.6 +/- 2.4 vs 20.0 +/- 1.4; P = 0.034 and 9.3 +/- 1.0 vs 5.9 +/- 1.1; P = 0.00003, respectively), and an improvement in ejection fraction (57.4 +/- 4.0 vs 72.6 +/- 3.8; P = 0.000007). The improvement in gallbladder emptying after cisapride therapy was confined to the patients with AN (n = 13) (57.3 +/- 5.4 vs 80.4 +/- 2.9; P = 0.0017), suggesting denervation supersensitivity with an upregulation of cholinergic receptors. There was no significant change in the ejection fraction in patients without AN (57.5 +/- 6.1 vs 65.4 +/- 6.5; P = NS). Sex, duration of diabetes, peripheral neuropathy, diabetic retinopathy and serum cholesterol level did not influence gallbladder emptying. Impaired gallbladder emptying is common in patients with type 2 DM. Cisapride significantly improves gallbladder emptying in patients with autonomic neuropathy.

Gallbladder muscle dysfunction in patients with chronic acalculous disease

Background & Aims: The mechanisms responsible for the abnormalities of gallbladder emptying in patients with chronic acalculous gallbladder disease (AGD) have not been elucidated. This study was designed to determine whether a muscle defect could explain this gallbladder dysfunction. Methods: Gallbladder contraction induced by a continuous intravenous cholecystokinin octapeptide (CCK-8) infusion was determined by ultrasonography in control subjects, patients with AGD, pigment stones, and cholesterol stones. Muscle cells were obtained by enzymatic digestion. 125I–CCK-8 binding and [35S]guanosine triphosphate γS (GTPγS) binding studies were performed. Results: In vivo gallbladder contraction induced by CCK-8 was significantly lower in AGD (29.4%) and cholesterol stones (28.8%) than in pigment stones (59.8%) and normal controls (57.8%; P < 0.01). In vitro muscle cell contraction induced by CCK-8 was also lower in AGD than in pigment stones. It remained impaired in AGD after stimulation with the G-protein activators GTPγS and AlF4 and with the second messenger 1,2-dioctanoyl-sn-glycerol. However, GTPγS binding induced by CCK-8 and vasoactive intestinal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment stones. Conclusions: These findings suggest that there is a good correlation between in vivo and in vitro gallbladder response to CCK-8 in patients with AGD. Unlike those found in cholesterol stones, the muscle defects in AGD appear to reside in the contractile apparatus.GASTROENTEROLOGY 2001;120:506-511

Cisapride improves gallbladder emptying in patients with diabetes

Cisapride improves gallbladder emptying in patients with diabetes

Gallbladder emptying in patients with liver cirrhosis is not impaired affer cabohydrates loading

Gallbladder emptying in patients with liver cirrhosis is not impaired affer cabohydrates loading

Bile lithogenicity and gallbladder emptying in patients with microlithiasis: Effect of bile acid therapy

Background & Aims: Biliary cholesterol supersaturation, rapid nucleation of cholesterol, and altered gallbladder motility are prerequisite for gallstone formation. However, the pathogenesis of microlithiasis is not clear. The aim of this study was to determine the abnormalities of gallbladder emptying and bile composition in patients with microlithiasis. Methods: Nucleation time, cholesterol saturation index (CSI), and gallbladder emptying were studied in patients with microlithiasis (n = 10), patients with gallstones (n = 10), and healthy volunteers (n = 10). Bile analysis was repeated in 6 patients with microlithiasis treated with ursodeoxycholic acid (UDCA) for 8 weeks. Results: Nucleation time was shorter in patients with microlithiasis and those with gallstones than in healthy volunteers ( P < 0.0001). Patients with microlithiasis had longer nucleation time than those with gallstones ( P < 0.001). There was no difference in cholesterol levels and CSI in gallstone and microlithiasis patients. However, healthy volunteers had lower cholesterol levels ( P < 0.01) and CSI ( P < 0.01). Patients with microlithiasis had prolongation of nucleation time ( P < 0.001) and lowering of CSI ( P < 0.001) after UDCA therapy. Gallbladder ejection fraction was higher in microlithiasis patients than in gallstone patients ( P < 0.01) but lower than in healthy volunteers ( P < 0.01). Conclusions: Patients with microlithiasis have longer nucleation time and better gallbladder emptying than patients with gallstones. Bile abnormalities can be successfully corrected with UDCA therapy in patients with microlithiasis. GASTROENTEROLOGY 1998;115:124-128

The effect of lanreotide therapy on gallbladder emptying in patients with acromegaly

The effect of lanreotide therapy on gallbladder emptying in patients with acromegaly

Effect of Cisapride on Gastroduodenal Reflux and Gall Bladder Motility in Patients with Gallstones

The aim of this work was to assess the effect of 10 mg of cisapride twice daily for 1 week on symptoms, gastroduodenal reflux and gall bladder emptying in patients undergoing cholecystectomy. Seventy-seven patients, 29 male and 48 female, underwent a randomized, double-blind, placebo-controlled trial with a 1-week treatment period between studies before cholecystectomy. Fifty-one of these patients were suitable for gall bladder emptying ejection fraction analysis. Gastroduodenal reflux and gall bladder emptying were assessed using Milk ⁹⁹Tc^m DIDA scans. Cisapride did not significantly alter gastroduodenal reflux but gall bladder motility was altered after cisapride treatment (p < 0.05).

Gallbladder motility and cholecystokinin secretion in chronic pancreatitis: relationship with exocrine pancreatic function

Background/Aims: Postprandial gallbladder motility is regulated mainly by the hormone cholecystokinin (CCK). Since CCK secretion may be reduced in patients with pancreatic insufficiency (PI), we studied postprandial gallbladder motility in these patients. Methods: Fifteen patients with PI due to chronic pancreatitis and 17 healthy control subjects were studied. Gallbladder volumes (ultrasonography) and plasma CCK concentrations (RIA) were determined at regular intervals for 120 min after meal ingestion. Urinary PABA and faecal fat excretion were measured to determine pancreatic exocrine function. Results: Patients with PI had larger fasting gallbladder volumes than controls (48±6 cm 3 versus 29±2 cm 3; p<0.01). Gallbladder ejection volume at time 120 min was not significantly different between patients with PI (14±4 cm 3) and controls (20±2 cm 3). However, the percentage postprandial gallbladder emptying in patients with PI was significantly reduced compared to controls (at 120 min; 29±8% versus 68±3%; p<0.001). Residual postprandial gallbladder volume was increased in patients with PI compared to controls (at 120 min: 34±4 cm 3 versus 9±1 cm 3; p<0.001). Postprandial endogenous CCK secretion was significantly reduced in patients with PI compared to controls (78±13 pM.120 min versus 155±14 pM.120 min; p<0.001). Postprandial gallbladder emptying (%) was related to the degree of exocrine pancreatic insufficiency ( r=0.81; p<0.001). Conclusions: In patients with pancreatic insufficiency due to chronic pancreatitis: 1) fasting and residual postprandial gallbladder volumes are significantly increased; 2) postprandial CCK secretion and percentage gallbladder contraction are significantly reduced; 3) percentage postprandial gallbladder emptying is related to the degree of pancreatic exocrine insufficiency.

Inhibitory effect of bile salts on gallbladder smooth muscle contractility in the guinea pig in vitro

BACKGROUND & AIMS: Impaired gallbladder emptying occurs in patients undergoing bile salt therapy for cholesterol gallstone dissolution and in patients with cirrhosis who have elevated serum bile salt concentrations. To determine if bile salts directly inhibit gallbladder contractility, isometric contraction of the guinea pig gallbladder was examined in vitro. METHODS: Contractile responses to cholecystokinin (CCK), bethanechol, KCI, and field stimulation were constructed alone and in the presence of selected bile salts: taurodeoxycholate (TDC), taurochenodeoxycholate, taurocholate, and tauroursodeoxycholate (TUDC). RESULTS: More hydrophobic bile salts, such as TDC (as low as 5 micromol/L), concentration-dependently depressed (P < 0.05) both CCK- and field stimulation-induced gallbladder contractions. More hydrophilic bile salts, such as TUDC, only caused a modest depression up to a concentration of 500 micromol/L. When 5 or 50 micromol/L of TUDC was added to the organ bath before the application of equalmolar TDC, the TDC-induced impaired gallbladder contractility was reversed. Thus, this inhibitory effect on gallbladder contraction depended on the hydrophobicity of bile salts and was also specific for certain stimuli such as CCK and field stimulation (mediated by cholinergic nerves, being abolished by atropine and tetrodotoxin). CONCLUSIONS: Such direct bile salt inhibition of CCK- and cholinergic nerve-induced gallbladder contraction may contribute to the deteriorating gallbladder emptying in patients undergoing bile salt therapy for stone dissolution and in cirrhotic patients who are at risk for gallstone formation. (Gastroenterology 1997 May;112(5):1699-706)