ArticleeGastroenterology2025
Ursodeoxycholic acid acts as an ileal FXR agonist in male mice with hepatic deficiency of FXR.
Article in eGastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Phytosterol-induced modulation of gut microbial bile salt hydrolases ameliorates hyperlipidemia via taurohyodeoxycholic acid-mediated FXR antagonism.Gut microbes · 2026Article
- Expanding bile acid diversityNatural product reports · 2026Review
- Bile acid signaling: from dynamic pool composition to inter-organ communication.Frontiers in endocrinology · 2026Review
- Association between gallstones and subclinical coronary atherosclerosis: An observational study with propensity score matching.PloS one · 2026Observational
- High-dose taurine supplementation exacerbates alcohol-associated liver disease by inducing gut microbiota dysbiosis and bile acid dysregulation in mice.eGastroenterology · 2026Article
- Liver fibrosis and cirrhosis in the multi-omics era: mechanisms and therapeutic perspectives from human and animal models.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Background: Farnesoid X receptor (FXR) has been identified as a therapeutic target for metabolic dysfunction-associated steatohepatitis (MASH). Hepatic FXR is especially critical in suppressing liver inflammation. FXR agonism and antagonism have both proven to be beneficial in the mitigation of MASH, leading to much controversy in the field, particularly regarding FXR signalling in the gut. The objective of this study was to determine the effects of ursodeoxycholic acid (UDCA), a postulated gut FXR antagonist with liver protective effects, on the mitigation and prevention of MASH development in mice with hepatic FXR deficiency. Methods: For this experiment, six-week-old to eight week-old male and female liver-specific FXR knockout (FXR Results: UDCA feeding tended to reduce alanine aminotransferase levels and decrease liver lipids in the male mice. Supplementation of UDCA showed a trend towards increased UDCA and tauroursodeoxycholic acid (TUDCA) levels in serum, liver and intestine, although the male mice displayed more than twice the amount of these bile acids compared with the female mice. CTL-UDCA feeding resulted in a significant induction of Conclusion: The data strongly suggest that UDCA seems to act as an FXR agonist, especially in the ileum, which contrasts with previous reports that UDCA acts as a gut FXR antagonist. In addition, UDCA seems to be exerting liver protective effects predominantly in the male mice.
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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 Socratic graph.