ArticleJHEP reports : innovation in hepatology2022
Bile acids contribute to the development of non-alcoholic steatohepatitis in mice.
Article in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.
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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
69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Pharmacological Mechanisms of Bile Acids Targeting the Farnesoid X Receptor.International journal of molecular sciences · 2024Pooled it
- Alterations in Circulating Bile Acids in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Systematic Review and Meta-Analysis.Biomolecules · 2023Pooled it
- Extract from Eucommia ulmoides Oliv. Leaves alleviates APAP-induced acute liver injury via reshaping gut microbiota and attenuating microbial bile acids metabolism disorder.Chinese medicine · 2026Article
- The Emerging Challenge of Non-Cirrhotic MASLD-Related Hepatocellular Carcinoma: Etiology, Immunopathology, and Precision Oncology.Liver cancer · 2026Review
- [Development and validation of a machine learning-based prediction model for fatty liver in Wilson disease].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Gut-liver metabolic and enterohormonal remodeling drives progression from metabolic dysfunction-associated steatotic liver disease to steatohepatitis.Metabolism: clinical and experimental · 2026Article
- The Multifaceted Roles of Gut Microbiota and Their Metabolites in Metabolic Dysfunction-associated Steatotic Liver Disease: A Literature Review.Journal of clinical and translational hepatology · 2026Review
- Bile acid signaling, metabolism, and aging.Liver research (Beijing, China) · 2026Review
- Targeting the intestinal barrier with traditional Chinese medicine for non-alcoholic fatty liver disease: mechanistic insights and therapeutic perspectives.Chinese medicine · 2026Review
- Enhanced nuclear localization of small heterodimer partner in metabolic dysfunction-associated steatohepatitis.JHEP reports : innovation in hepatology · 2026Article
- Bile acids and bile acid modification in health and disease: from novel modifications to therapeutic interventions.Frontiers in endocrinology · 2026Review
- Gut microbial bile salt hydrolase as a metabolic gatekeeper in digestive homeostasis and disease.Frontiers in immunology · 2026Review
- The role of bile acid-activated receptor TGR5 in inflammation and liver diseases.Frontiers in physiology · 2026Review
- The gut microbiota-bile acid-FXR axis in NAFLD: from progression to therapeutic applications.Frontiers in physiology · 2026Review
- Mechanisms underlying the role of the oral-gut-liver axis in the promotion of liver fibrosis by periodontal disease: an interacting network of inflammation, microbiota, and barrier function.Frontiers in cellular and infection microbiology · 2026Review
- Superior inflammatory response and MASH progression inFrontiers in immunology · 2026Article
- Gut microbiota in hepatocellular carcinoma immunotherapy: immune microenvironment remodeling and gut microbiota modification.Gut microbes · 2025Review
- A Mediterranean Diet-Based Food Mix Ameliorates Diabetes- and Obesity-Associated Liver Alterations Through Mitochondrial and Metabolic Reprogramming.Molecular nutrition & food research · 2025Article
- Metabolomic, Lipidomic, and Enterohormone Changes in the Progression from MASLD to MASH.bioRxiv : the preprint server for biology · 2025Article
- Exercise-Induced Changes in Enterohepatic Communication Are Linked to Liver Steatosis Resolution.Nutrients · 2025Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsThrough FXR and TGR5 signaling, bile acids (BAs) modulate lipid and glucose metabolism, inflammation and fibrosis. Hence, BAs returning to the liver after enteric secretion, modification and reabsorption may contribute to the pathogenesis of non-alcoholic steatohepatitis (NASH). Herein, we characterized the enterohepatic profile and signaling of BAs in preclinical models of NASH, and explored the consequences of experimental manipulation of BA composition.
methodsWe used high-fat diet (HFD)-fed
resultsCompared to controls, mice with NASH had lower concentrations of BAs in their portal blood and bile, while systemic BA concentrations were not significantly altered. Notably, the concentrations of secondary BAs, and especially of DCA, and the ratio of secondary to primary BAs were strikingly lower in bile and portal blood of mice with NASH. Hence, portal blood was poor in FXR and TGR5 ligands, and conferred poor anti-inflammatory protection in mice with NASH. Enhanced primary BAs synthesis and conversion of secondary to primary BAs in NASH livers contributed to the depletion in secondary BAs. Dietary DCA supplementation in HFD-fed
conclusionsBA composition in the enterohepatic cycle, but not in systemic circulation, is profoundly altered in preclinical models of NASH, with specific depletion in secondary BAs. Dietary correction of the BA profile protected from NASH, supporting a role for enterohepatic BAs in the pathogenesis of NASH. LAY SUMMARY: This study clearly demonstrates that the alterations of enterohepatic bile acids significantly contribute to the development of non-alcoholic steatohepatitis in relevant preclinical models. Indeed, experimental modulation of bile acid composition restored perturbed FXR and TGR5 signaling and prevented non-alcoholic steatohepatitis and associated metabolic disorders.
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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.