ArticleEuropean journal of clinical investigation2016
The cholecystokinin-1 receptor antagonist devazepide increases cholesterol cholelithogenesis in mice.
Article in European journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- NLRP3 Inflammasome Activation-Induced Acute Papillitis as a Trigger of Acute Pancreatitis - A Novel Mechanism of Microlithiasis-Induced Acute Pancreatitis.United European gastroenterology journal · 2026Article
- Calcium and Neural Stem Cell Proliferation.International journal of molecular sciences · 2024Review
- Effects of Biliary Phospholipids on Cholesterol Crystallization and Growth in Gallstone Formation.Advances in therapy · 2023Review
- Review
- Physical Activity Modulating Lipid Metabolism in Gallbladder Diseases.Journal of gastrointestinal and liver diseases : JGLD · 2020Review
- Update on the Molecular Mechanisms Underlying the Effect of Cholecystokinin and Cholecystokinin-1 Receptor on the Formation of Cholesterol Gallstones.Current medicinal chemistry · 2019Review
- Similarities and differences between biliary sludge and microlithiasis: Their clinical and pathophysiological significances.Liver research (Beijing, China) · 2018Article
- An update on the pathogenesis of cholesterol gallstone disease.Current opinion in gastroenterology · 2018Review
- Mouse models of gallstone disease.Current opinion in gastroenterology · 2018Review
Corrections and comments
- Commented on by
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundA defect in gallbladder contraction function plays a key role in the pathogenesis of gallstones. The cholecystokinin-1 receptor (CCK-1R) antagonists have been extensively investigated for their therapeutic effects on gastrointestinal and metabolic diseases in animal studies and clinical trials. However, it is still unknown whether they have a potential effect on gallstone formation.
designTo study whether the CCK-1R antagonists enhance cholelithogenesis, we investigated cholesterol crystallization, gallstone formation, hepatic lipid secretion, gallbladder emptying function and intestinal cholesterol absorption in male C57BL/6J mice treated by gavage with devazepide (4 mg/day/kg) or vehicle (as controls) twice per day and fed the lithogenic diet for 21 days.
resultsDuring 21 days of feeding, oral administration of devazepide significantly accelerated cholesterol crystallization and crystal growth to microlithiasis, with 40% of mice forming gallstones, whereas only agglomerated cholesterol monohydrate crystals were found in mice receiving vehicle. Compared to the vehicle group, fasting and postprandial residual gallbladder volumes in response to the high-fat meal were significantly larger in the devazepide group during cholelithogenesis, showing reduced gallbladder emptying and bile stasis. Moreover, devazepide significantly increased hepatic secretion of biliary cholesterol, but not phospholipids or bile salts. The percentage of intestinal cholesterol absorption was higher in devazepide-treated mice, increasing the bioavailability of chylomicron-derived cholesterol in the liver for biliary hypersecretion into bile. These abnormalities induced supersaturated bile and rapid cholesterol crystallization.
conclusionsThe potent CCK-1R antagonist devazepide increases susceptibility to gallstone formation by impairing gallbladder emptying function, disrupting biliary cholesterol metabolism and enhancing intestinal cholesterol absorption in mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.