ArticleJournal of lipid research2016
Cyp2c70 is responsible for the species difference in bile acid metabolism between mice and humans.
Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 2 of them syntheses that pooled it.
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Who cites it
174 citing papers in PubMed, 2 syntheses or guidelines pooled it, 296 citations in OpenAlex.
- Bile Acids Transporters of Enterohepatic Circulation for Targeted Drug Delivery.Molecules (Basel, Switzerland) · 2022Pooled it
- Bile Acids and FXR: Novel Targets for Liver Diseases.Frontiers in medicine · 2020Pooled it
- Lithocholic acid alleviates fatty liver in mice and non-human primate macaques.Life metabolism · 2026Article
- Targeting microbial bile salt hydrolase reprograms bile acid metabolism and ameliorates metabolic dysfunction-associated steatohepatitis in mice.Molecular metabolism · 2026Article
- The Human Microbiome in Airborne Particulate Matter-Associated Aging-Related Chronic Diseases: An Evidence-Stratified Review.Environment & health (Washington, D.C.) · 2026Review
- Modulating Host Lipid Metabolism via Gut Microbiota: Therapeutic Potential of Plant-Derived Compounds.Phytotherapy research : PTR · 2026Review
- The effect of rocking speed and cell inoculation density on hepatic spheroid size: A simple method for size modulation.Bioengineering & translational medicine · 2026Article
- Hepatic FXR deficiency exacerbates dyslipidemia by disrupting the gut-liver axis via bile acid disorder and gut microbiota dysbiosis.Journal of translational medicine · 2026Article
- Lithocholic acid-activated VDR in macrophages promotes HCC recurrence post-ablation via SOCS3-mediated suppression of CXCL16.Journal for immunotherapy of cancer · 2026Article
- Chenodeoxycholic acid redirects the bile acid synthetic pathway to limit pro-inflammatory neutrophil infiltration and alleviate colitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Ecology and engineering to modify the bile acid output of a defined microbial community.bioRxiv : the preprint server for biology · 2026Article
- Nanosecond Infrared Laser Sampling of Mouse and Human Liver Tissues for LC-MS/MS Analysis of Bile Acids.International journal of molecular sciences · 2026Article
- The conjugation-resistant bile acid norUDCA cures liver fibrosis but impairs systemic energy metabolism.Molecular metabolism · 2026Article
- Deficiency of ZFP36L1 and ZFP36L2 impairs liver homeostasis and initiates cholestatic liver injury.Hepatology communications · 2026Article
- The influence and mechanism of gut microbiota on spermatogenesis.Cell biology and toxicology · 2026Review
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- Bile acids regulate lipid metabolism through selective actions on fatty acid absorption.Cell metabolism · 2026Article
- The gut microbiota-bile acid-FXR axis in NAFLD: from progression to therapeutic applications.Frontiers in physiology · 2026Review
- Cholestasis in Alcohol-Associated Liver Disease.The American journal of pathology · 2026Review
- Bile acid signaling: from dynamic pool composition to inter-organ communication.Frontiers in endocrinology · 2026Review
114 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Bile acids are synthesized from cholesterol in the liver and subjected to multiple metabolic biotransformations in hepatocytes, including oxidation by cytochromes P450 (CYPs) and conjugation with taurine, glycine, glucuronic acid, and sulfate. Mice and rats can hydroxylate chenodeoxycholic acid (CDCA) at the 6β-position to form α-muricholic acid (MCA) and ursodeoxycholic acid (UDCA) to form β-MCA. However, MCA is not formed in humans to any appreciable degree and the mechanism for this species difference is not known. Comparison of several Cyp-null mouse lines revealed that α-MCA and β-MCA were not detected in the liver samples from Cyp2c-cluster null (Cyp2c-null) mice. Global bile acid analysis further revealed the absence of MCAs and their conjugated derivatives, and high concentrations of CDCA and UDCA in Cyp2c-null mouse cecum and feces. Analysis of recombinant CYPs revealed that α-MCA and β-MCA were produced by oxidation of CDCA and UDCA by Cyp2c70, respectively. CYP2C9-humanized mice have similar bile acid metabolites as the Cyp2c-null mice, indicating that human CYP2C9 does not oxidize CDCA and UDCA, thus explaining the species differences in production of MCA. Because humans do not produce MCA, they lack tauro-β-MCA, a farnesoid X receptor antagonist in mouse that modulates obesity, insulin resistance, and hepatosteatosis.
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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.