ArticleEuropean journal of clinical investigation2015
Endogenous elevation of plasma cholecystokinin does not prevent gallstones.
Article in European journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice.PloS one · 2025Article
- Cholecystokinin and cholecystokinin-A receptor: An attractive treatment strategy for biliary dyskinesia?World journal of gastroenterology · 2024Article
- The preference for sugar over sweetener depends on a gut sensor cell.Nature neuroscience · 2022Article
- Obesity and Gallstones.Visceral medicine · 2021Review
- Rodent models of cholestatic liver disease: A practical guide for translational research.Liver international : official journal of the International Association for the Study of the Liver · 2021Review
- Prevention of gallbladder hypomotility via FATP2 inhibition protects from lithogenic diet-induced cholelithiasis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- The cholecystokinin-1 receptor antagonist devazepide increases cholesterol cholelithogenesis in mice.European journal of clinical investigation · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRegular gall bladder contraction reduces bile stasis and prevents gallstone formation. Intraduodenal administration of exogenous pancreatic secretory trypsin inhibitor-I (PSTI-I, also known as monitor peptide) causes cholecystokinin (CCK) secretion.
designWe proposed that stimulation of CCK release by PSTI would produce gall bladder contraction and prevent gallstones in mice fed a lithogenic diet. Therefore, we tested the effect of overexpression of rat PSTI-I in pancreatic acinar cells on plasma CCK levels and gall bladder function in a transgenic mouse line (TgN[Psti1]; known hereafter as PSTI-I tg).
resultsImportantly, PSTI tg mice had elevated fasting and fed plasma CCK levels compared to wild-type (WT) mice. Only mice fed the lithogenic diet developed gallstones. Both fasting and stimulated plasma CCK levels were substantially reduced in both WT and PSTI-I tg mice on the lithogenic diet. Moreover, despite higher CCK levels PSTI-I tg animals developed more gallstones than WT animals.
conclusionsTogether with the previously observed decrease in CCK-stimulated gall bladder emptying in mice fed a lithogenic diet, our findings suggest that a lithogenic diet causes gallstone formation by impaired CCK secretion in addition to reduced gall bladder sensitivity to CCK.
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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.