ArticleToxicology and applied pharmacology2015
Individual bile acids have differential effects on bile acid signaling in mice.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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.
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Who cites it
47 citing papers in PubMed, 94 citations in OpenAlex.
- Role of gut microbiota metabolites in maintaining intestinal health and preventing weaning-associated diarrhea in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Review
- White Adipose Tissue as a Functional Target of Secondary Bile Acids in Rainbow Trout (Oncorhynchus mykiss).Marine biotechnology (New York, N.Y.) · 2026Article
- Ursodeoxycholic acid as a potential cardioprotective agent: molecular mechanisms, experimental evidence, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Yinchenhao Decoction Mitigates Cholestatic Liver Injury in Mice via Gut Microbiota Regulation and Activation of FXR-FGF15 Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Double-negative T cells in combination with ursodeoxycholic acid ameliorates immune-mediated cholangitis in mice.BMC medicine · 2025Article
- Bioinformatics based exploration of the anti-NAFLD mechanism of Wang's empirical formula via TLR4/NF-κB/COX2 pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Effects of therapeutically approved individual bile acids on the development of metabolic dysfunction-associated steatohepatitis a low bile acid mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Hepatic protein phosphatase 1 regulatory subunit 3G alleviates obesity and liver steatosis by regulating the gut microbiota and bile acid metabolism.Journal of pharmaceutical analysis · 2024Article
- Characterization of individual bile acids in vivo utilizing a novel low bile acid mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Bile acids and coronavirus disease 2019.Acta pharmaceutica Sinica. B · 2024Review
- Article
- Glycocholic acid supplementation improved growth performance and alleviated tissue damage in the liver and intestine in Pelteobagrus fulvidraco fed a high-pectin diet.Fish physiology and biochemistry · 2024Article
- Enhancing milk quality and modulating rectal microbiota of dairy goats in starch-rich diet: the role of bile acid supplementation.Journal of animal science and biotechnology · 2024Article
- Quantitative bile acid profiling in healthy adult dogs and pups from serum, plasma, urine, and feces using LC-MS/MS.Frontiers in veterinary science · 2024Article
- Carvedilol impairs bile acid homeostasis in mice: implication for nonalcoholic steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Emerging Roles of Gut Microbial Modulation of Bile Acid Composition in the Etiology of Cardiovascular Diseases.Nutrients · 2023Review
- The Black Box Orchestra of Gut Bacteria and Bile Acids: Who Is the Conductor?International journal of molecular sciences · 2023Review
- Bile Acids-A Peek Into Their History and Signaling.Endocrinology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bile acids (BAs) are known to regulate BA synthesis and transport by the farnesoid X receptor in the liver (FXR-SHP) and intestine (FXR-Fgf15). However, the relative importance of individual BAs in regulating these processes is not known. Therefore, mice were fed various doses of five individual BAs, including cholic acid (CA), chenodeoxycholic acid (CDCA), deoxoycholic acid (DCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA) in their diets at various concentrations for one week to increase the concentration of one BA in the enterohepatic circulation. The mRNA of BA synthesis and transporting genes in liver and ileum were quantified. In the liver, the mRNA of SHP, which is the prototypical target gene of FXR, increased in mice fed all concentrations of BAs. In the ileum, the mRNA of the intestinal FXR target gene Fgf15 was increased at lower doses and to a higher extent by CA and DCA than by CDCA and LCA. Cyp7a1, the rate-limiting enzyme in BA synthesis, was decreased more by CA and DCA than CDCA and LCA. Cyp8b1, the enzyme that 12-hydroxylates BAs and is thus responsible for the synthesis of CA, was decreased much more by CA and DCA than CDCA and LCA. Surprisingly, neither a decrease in the conjugated BA uptake transporter (Ntcp) nor increase in BA efflux transporter (Bsep) was observed by FXR activation, but an increase in the cholesterol efflux transporter (Abcg5/Abcg8) was observed with FXR activation. Thus in conclusion, CA and DCA are more potent FXR activators than CDCA and LCA when fed to mice, and thus they are more effective in decreasing the expression of the rate limiting gene in BA synthesis Cyp7a1 and the 12-hydroxylation of BAs Cyp8b1, and are also more effective in increasing the expression of Abcg5/Abcg8, which is responsible for biliary cholesterol excretion. However, feeding BAs do not alter the mRNA or protein levels of Ntcp or Bsep, suggesting that the uptake or efflux of BAs is not regulated by FXR at physiological and pharmacological concentrations of BAs.
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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.