Cited by 737Drug Transport and Resistance MechanismsLiver Disease Diagnosis and TreatmentGut microbiota and health

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Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD

Jiao, Na, Baker, Susan S, Chapa-Rodriguez, Adrian, Liu, Wensheng, Nugent, Colleen A, Tsompana, Maria, Mastrandrea, Lucy, Buck, Michael J, Baker, Robert D, Genco, Robert J, Zhu, Ruixin, Zhu, Lixin·2018·Gut

DOI 10.1136/gutjnl-2017-314307

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Abstract

OBJECTIVE: Bile acids are regulators of lipid and glucose metabolism, and modulate inflammation in the liver and other tissues. Primary bile acids such as cholic acid and chenodeoxycholic acid (CDCA) are produced in the liver, and converted into secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid by gut microbiota. Here we investigated the possible roles of bile acids in non-alcoholic fatty liver disease (NAFLD) pathogenesis and the impact of the gut microbiome on bile acid signalling in NAFLD. DESIGN: Serum bile acid levels and fibroblast growth factor 19 (FGF19), liver gene expression profiles and gut microbiome compositions were determined in patients with NAFLD, high-fat diet-fed rats and their controls. RESULTS: -taurocholate cotransporting polypeptide and paraoxonase 1, no change in mRNA expression for small heterodimer partner and bile salt export pump, and reduced serum FGF19 were evidence of impaired FXR and fibroblast growth factor receptor 4 (FGFR4)-mediated signalling in NAFLD. Taurine and glycine metabolising bacteria were increased in the gut of patients with NAFLD, reflecting increased secondary bile acid production. Similar changes in liver gene expression and the gut microbiome were observed in high-fat diet-fed rats. CONCLUSIONS: The serum bile acid profile, the hepatic gene expression pattern and the gut microbiome composition consistently support an elevated bile acid production in NAFLD. The increased proportion of FXR antagonistic bile acid explains, at least in part, the suppression of hepatic FXR-mediated and FGFR4-mediated signalling. Our study suggests that future NAFLD intervention may target the components of FXR signalling, including the bile acid converting gut microbiome.

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Background
Paeoniflorin alleviates 17α-ethinylestradiol-induced cholestasis via the farnesoid X receptor-mediated bile acid homeostasis signaling pathway in rats
Wang, R., Yuan, T., Sun, J., Yang, M., Chen, Y., Wang, L., Wang, Y., Chen, W., & Peng, D. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.1064653 · Cited by 4
“Primary bile acids are converted to secondary bile acids by the action of intestinal flora (Jiao et al., 2018).”
Background
Disrupting Osr1 expression promoted hepatic steatosis and inflammation induced by high-fat diet in the mouse model
Lynch, E. C., Liu, Z., Liu, L., Wang, X., Zhang, K. K., & Xie, L. (2022) · PLoS ONE · doi:10.1371/journal.pone.0268344 · Cited by 4
“Dysregulation of this feedback signaling network significantly contributes to pathologies of NAFLD [27, 28].”
Background
Gut-muscle communication links FGF19 levels to the loss of lean muscle mass following rapid weight loss
Wean, J., Baranwal, S., Miller, N., Shin, J. H., O’Rourke, R. W., Burant, C., Seeley, R. J., Rothberg, A. E., & Bozadjieva-Kramer, N. (2024) · Diabetes & Metabolism · doi:10.1016/j.diabet.2024.101570 · Cited by 4
Effects of dietary supplementation with oleic acid on growth performance, dietary fat utilization, serum and intestinal lipid metabolic parameters, and enterocyte lipid droplet metabolism in Pekin ducks
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“However, diets enriched with excessive oil may not be fully digested and absorbed due to the limited secretion of lipase and bile acids (BAs) in ducks, potentially resulting in dietary lipid wastage (de Melo et al., 2017; Jiao et al., 2018; Zeng et al., 2023; Wei et al., 2024).”
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Qushi Huayu decoction alleviates NAFLD in mice by regulating gut microbiota homeostasis in the gut-liver axis via the pregnane X receptor
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“However, DCA may act as a pro-inflammatory FXR antagonist in the presence of chenodeoxycholic acid [32].”
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“Secondary bile acids (SBAs)— including deoxycholic acid (DCA) and lithocholic acid (LCA)—are generated from primary bile acids exclusively through the enzymes produced by gut bacteria and are now recognized as important immunomodulators (Fu et al., 2025; Jiao et al., 2018).”
Self-citation
Decoding the Gut-Liver Crosstalk: Microbial Metabolite- Driven AhR Signalling Networks in MASLD Pathogenesis
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ResultInfluential
Bile Acids: A Bridge Linking Gut Microbiota and NAFLD
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BackgroundResultInfluential
Gut Microbiome and Liver Diseases from the Perspective of 3PM: The Predictive, Preventive, and Personalized Medicine
Skladaný, Ľ., Koller, T., Kukla, M., & Šoltýs, K. (2023) · Advances in predictive, preventive and personalised medicine · doi:10.1007/978-3-031-34884-6_9 · Cited by 3
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Nuclear Receptors and Lipid Sensing
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“serum bile acid composition in NAFLD patients, an increase in FXR antagonists and a decrease in FXR agonists levels were reported (16).”
Background
Regulation of Hepatocyte Nuclear Factor 4α Attenuated Lipotoxicity but Increased Bile Acid Toxicity in Non-Alcoholic Fatty Liver Disease
Roh, Y. J., Kim, Y., Lee, J. S., Oh, J., Lee, S. M., Yoon, E. L., Lee, S. R., & Jun, D. W. (2022) · Life · doi:10.3390/life12111682 · Cited by 3
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BackgroundResultInfluential
An Atlas of Inter-Organ Metabolite Trafficking in Health and Atherogenic ConditionsPreprint
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Disrupted host-microbiota crosstalk promotes nonalcoholic fatty liver disease progression by impaired mitophagy
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“For example, our previous work demonstrated how gut microbiota contributes to NAFLD by elevating secondary bile acids that suppress hepatic FXR signaling (20).”
Self-citation
Integration of Pseudotargeted Metabolomics and Microbiomics Reveals That Hugan Tablets Ameliorate NASH with Liver Fibrosis in Mice by Modulating Bile Acid Metabolism via the Gut Microbiome
Dong, W., Wang, Y., Li, H., Ma, H., Gong, Y., Luo, G., & Gao, X. (2025) · Metabolites · doi:10.3390/metabo15070433 · Cited by 2
Taurochenodeoxycholic acid as a sensitive stratification marker for HBV-associated hepatic cirrhosis status has a hepatoprotective effect
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Self-citation
Liuwei Dihuang Formula ameliorates glycolipid metabolism in type 2 diabetic rats through an integrated analysis of gut microbiota and bile acids
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Bile Acid Supplementation Reduced Hepatic Lipid Deposition and Modulated Bile Acid Metabolism and the Gut Microbiota in Weaned Piglets
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EGCG alleviates colitis in inflammatory bowel disease via gut microbiota-derived LCA and inhibition of NLRP3 inflammasome
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“For example, elevated levels of total secondary BAs and especially DCA have been linked to NAFLD and non-alcoholic steatohepatitis (NASH) [31].”
Xiayuxue decoction alleviates MASH by regulating gut microbiota, bile acid metabolism, and m6A modification
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Dietary anthocyanins alleviate age-dependent hepatic steatosis by expanding Limosilactobacillus reuteri and modulating gut microbiota–bile acid–hepatic FXR signaling
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Current advances in restoring intestinal barrier homeostasis by natural medicines
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Isoquercetin Ameliorates Obesity-Associated Muscle Atrophy and Modulates the Gut Microbiota–Bile Acid Axis
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UPLC-Q-TOF/MS-Based Metabolomics and 16S rRNA Profiling Reveal that Corosolic Acid Ameliorates High-Fat Diet-Induced MASLD by Modulating the Gut-Liver Axis to Inhibit the cGAS-STING Pathway
Cai, K., Chen, Z., Deng, S., Chen, J., Yu, J., Zhang, X., Jia, W. P., Huang, A., Chen, Y., Xie, Z., et al. (2026) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.5c13513 · Cited by 2

Authors: Jiao, N., Baker, S. S., Chapa-Rodriguez, A., Liu, W., Nugent, C. A., Tsompana, M., Mastrandrea, L., Buck, M. J., Baker, R. D., Genco, R. J., Zhu, R., & Zhu, L.
Affiliations: Tongji University (CN)
University at Buffalo, State University of New York (US)
Department of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA
Corresponding author: Baker, Susan S
Zhu, Lixin
ORCID: Jiao, Na
Baker, Susan S
Liu, Wensheng
Nugent, Colleen A
Tsompana, Maria
Mastrandrea, Lucy
Buck, Michael J
Genco, Robert J
Zhu, Ruixin
Zhu, Lixin
Venue: Gut
Publisher: BMJ
Published: 2017-08-03
Volume: 67
Issue: 10
Pages: 1881-1891
ISSN: 0017-5749 (ISSN-L)
1468-3288
DOI: 10.1136/gutjnl-2017-314307
OpenAlex: W2605955022
Cited by: 737
References: 50
Citations by year: 2026: 81 · 2025: 112 · 2024: 128 · 2023: 105 · 2022: 93 · 2021: 83 · 2020: 68 · 2019: 44 · 2018: 17 · 2017: 4
FWCI: 15.93
Type: journal article
Language: en
Open access: closed
Locations: Gut (publishedVersion)
PubMed (publishedVersion)
HighWire Press Open Archive (submittedVersion)
Funders: GEM Community of Excellence, the University at Buffalo
the University at Buffalo Departmental Start-Up Fund
Natural Science Foundation of Shanghai
National Natural Science Foundation of China
the Peter and Tommy Fund, Inc., Buffalo, NY
Topics: Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
Keywords: non-alcoholic fatty liver disease, bile acids, bile acid signaling, farnesoid X receptor, FGFR4, FGF19, gut microbiota, secondary bile acids, deoxycholic acid, lithocholic acid, taurine metabolism, hepatic gene expression, high-fat diet
MeSH terms: Gastrointestinal Microbiome, Receptor, Farnesoid X-Activated, Animals, Bile Acids and Salts, Cholesterol 7-alpha-Hydroxylase, Female, Fibroblast Growth Factors, Humans, Male, Middle Aged, Signal Transduction, Receptors, Cytoplasmic and Nuclear, Gene Expression Profiling, Rats, Diet, High-Fat, Non-alcoholic Fatty Liver Disease

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Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD

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