ArticleInternational journal of molecular sciences2022
Systemic Bile Acids Affect the Severity of Acute Pancreatitis in Mice Depending on Their Hydrophobicity and the Disease Pathogenesis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Odoribacter laneus protects intestinal barrier by bile acid-FXR axis in acute pancreatitis.AMB Express · 2026Article
- 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
- Hyperoside modulates bile acid and fatty acid metabolism, presenting a potentially promising treatment for non-alcoholic fatty liver disease.Journal of advanced research · 2026Article
- Exploring the Role of Gut Microbiota and Probiotics in Acute Pancreatitis: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Integrating metagenomics with metabolomics for gut microbiota and metabolites profiling in acute pancreatitis.Scientific reports · 2024Article
- The Role of the Gut Microbiome in the Development of Acute Pancreatitis.International journal of molecular sciences · 2024Review
- L-Arginine-induced acute pancreatitis and its associated lung injury in rats: Down-regulation of TLR-4/MAPK-p38/JNK signaling pathway viaIranian journal of basic medical sciences · 2024Article
- The Interaction of Microbiome and Pancreas in Acute Pancreatitis.Biomolecules · 2023Review
- Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis.Cell reports. Medicine · 2023Article
- Photodynamic Activation of Cholecystokinin 1 Receptor Is Conserved in Mammalian and Avian Pancreatic Acini.Biomedicines · 2023Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute pancreatitis (AP) is a major, globally increasing gastrointestinal disease and a biliary origin is the most common cause. However, the effects of bile acids (BAs), given systemically, on the pancreas and on disease severity remains elusive. In this study, we have investigated the roles of different circulating BAs in animal models for AP to elucidate their impact on disease severity and the underlying pathomechanisms. BAs were incubated on isolated acini and AP was induced through repetitive injections of caerulein or L-arginine; pancreatic duct ligation (PDL); or combined biliopancreatic duct ligation (BPDL). Disease severity was assessed using biochemical and histological parameters. Serum cholecystokinin (CCK) concentrations were determined via enzyme immunoassay. The binding of the CCK1 receptor was measured using fluorescence-labeled CCK. In isolated acini, hydrophobic BAs mitigated the damaging effects of CCK. The same BAs further enhanced pancreatitis in L-arginine- and PDL-based pancreatitis, whereas they ameliorated pancreatic damage in the caerulein and BPDL models. Mechanistically, the binding affinity of the CCK1 receptor was significantly reduced by hydrophobic BAs. The hydrophobicity of BAs and the involvement of CCK seem to be relevant in the course of AP. Systemic BAs may affect the severity of AP by interfering with the CCK1 receptor.
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Registered trials
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