The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
The presence and severity of nonalcoholic steatohepatitis is associated with specific changes in circulating bile acids
Open accessAbstract
The histologic spectrum of nonalcoholic fatty liver disease (NAFLD) includes fatty liver (NAFL) and steatohepatitis (NASH), which can progress to cirrhosis in up to 20% of NASH patients. Bile acids (BA) are linked to the pathogenesis and therapy of NASH. We (1) characterized the plasma BA profile in biopsy‐proven NAFL and NASH and compared to controls and (2) related the plasma BA profile to liver histologic features, disease activity, and fibrosis. Liquid chromatography/mass spectrometry quantified BAs. Descriptive statistics, paired and multiple group comparisons, and regression analyses were performed. Of 86 patients (24 controls, 25 NAFL, and 37 NASH; mean age 51.8 years and body mass index 31.9 kg/m 2), 66% were women. Increased total primary BAs and decreased secondary BAs (both P < 0.05) characterized NASH. Total conjugated primary BAs were significantly higher in NASH versus NAFL (P = 0.047) and versus controls (P < 0.0001). NASH had higher conjugated to unconjugated chenodeoxycholate (P = 0.04), cholate (P = 0.0004), and total primary BAs (P < 0.0001). The total cholate to chenodeoxycholate ratio was significantly higher in NAFLD without (P = 0.005) and with (P = 0.02) diabetes. Increased key BAs were associated with higher grades of steatosis (taurocholate), lobular (glycocholate) and portal inflammation (taurolithocholate), and hepatocyte ballooning (taurocholate). Conjugated cholate and taurocholate directly and secondary to primary BA ratio inversely correlated to NAFLD activity score. A higher ratio of total secondary to primary BA decreased (odds ratio, 0.57; P = 0.004) and higher conjugated cholate increased the likelihood of significant fibrosis (F≥2) (P = 0.007). Conclusion: NAFLD is associated with significantly altered circulating BA composition, likely unaffected by type 2 diabetes, and correlated with histological features of NASH; these observations provide the foundation for future hypothesis‐driven studies of specific effects of BAs on specific aspects of NASH. (H epatology 2018;67:534‐548).
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“These BA (DCA, TCDCA, GCDCA) are significantly increased in patients with NASH [247].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [247]
In the citing paper
“Increased circulating DCA levels have been found in patients with NASH [247].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [247]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Design and validation of a histological scoring system for nonalcoholic fatty liver disease†
Kleiner, D. E., Brunt, E. M., Van Natta, M., Behling, C., Contos, M. J., Cummings, O. W., Ferrell, L. D., Liu, Y., Torbenson, M. S., Unalp‐Arida, A., et al. (2005) · Hepatology · doi:10.1002/hep.20701 · Cited by 10,791
Self-citationDonnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23621 · Cited by 3,604
Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity.
MATTEONI, C., YOUNOSSI, Z., GRAMLICH, T., BOPARAI, N., LIU, Y., & MCCULLOUGH, A. (1999) · Gastroenterology · doi:10.1016/s0016-5085(99)70506-8 · Cited by 3,345
Bile salt biotransformations by human intestinal bacteria
Ridlon, J. M., Kang, D.-J., & Hylemon, P. B. (2006) · Journal of Lipid Research · doi:10.1194/jlr.r500013-jlr200 · Cited by 2,829
Self-citationIdentification of a nuclear receptor for bile acids
Makishima, M., Okamoto, A. Y., Repa, J. J., Tu, H., Learned, R. M., Luk, A., Hull, M. V., Lustig, K. D., Mangelsdorf, D. J., & Shan, B. (1999) · Science · doi:10.1126/science.284.5418.1362 · Cited by 2,714
Nonalcoholic Fatty Liver Disease
Rinella, M. E. (2015) · JAMA · doi:10.1001/jama.2015.5370 · Cited by 2,320
Neuschwander-Tetri, B. A., Loomba, R., Sanyal, A. J., Lavine, J. E., Van Natta, M. L., Abdelmalek, M. F., Chalasani, N., Dasarathy, S., Diehl, A. M., Hameed, B., et al. (2015) · The Lancet · doi:10.1016/s0140-6736(14)61933-4 · Cited by 2,237
Self-citationNonalcoholic steatohepatitis: association of insulin resistance and mitochondrial abnormalities
Sanyal, A. J., Campbell–Sargent, C., Mirshahi, F., Rizzo, W. B., Contos, M. J., Sterling, R. K., Luketic, V. A., Shiffman, M. L., & Clore, J. N. (2001) · Gastroenterology · doi:10.1053/gast.2001.23256 · Cited by 2,078
Self-citationTGR5-Mediated Bile Acid Sensing Controls Glucose Homeostasis
Thomas, C., Gioiello, A., Noriega, L., Strehle, A., Oury, J., Rizzo, G., Macchiarulo, A., Yamamoto, H., Mataki, C., Pruzanski, M., et al. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.08.001 · Cited by 1,885
Wong, R. J., Aguilar, M. E. F., Cheung, R. C., Perumpail, R. B., Harrison, S. A., Younossi, Z. M., & Ahmed, A. (2014) · Gastroenterology · doi:10.1053/j.gastro.2014.11.039 · Cited by 1,861
Flagged first, then by citations
Cited by
Sorted by citations
Items 401–424 of 424
Rôle de LECT2 dans les maladies stéatosiques non alcooliques du foie
Pham, S. (2020) · theses.fr (ABES) · doi:10.70675/3693bfe6z9d91z4045za9a9zc37497dc9c1b
Influence du sexe dans la susceptibilité aux hépatopathies métaboliques
Smati, S. (2019) · theses.fr (ABES) · doi:10.70675/01997f55za990z41e6z96baz8221de2a6281
Rôle du récepteur Farnesoid X dans le contrôle central de l'homéostasie énergétique
Deckmyn, B. (2022) · theses.fr (ABES) · doi:10.70675/db76bb16z01f4z4f26zaf99za1003045be0c
Inter-organ communication in physiology and pathophysiology : a role for the ChREBP-FGF21 axis?
Carbinatti, T. (2024) · theses.fr (ABES) · doi:10.70675/5d147ab4zad37z4f6bzac51z32a08efeaa51
Rôle de FAT10 dans la sénescence des hépatocytes et le développement de la NASH
Bernard, L. (2023) · theses.fr (ABES) · doi:10.70675/793b0b93z9794z42d4zb8dfz5f3d68268a9b
Lv, Q., Guan, Y., Bai, X., Wang, X., & Jiang, B. (2026) · Chinese Herbal Medicines · doi:10.1016/j.chmed.2026.04.002
Wu, Q., Gao, L.-Y., Feng, H., Liu, H.-L., Gao, H., Peng, W., & Li, N. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1797381
The association between primary bile acids and metabolically unhealthy obesity
Zong, M., Wu, C., Zhao, S., Kong, L., Li, W., Shi, J., Chen, Y., Ye, Y., Gao, A., Ning, G., et al. (2026) · Diabetes & Metabolism · doi:10.1016/j.diabet.2026.101761
Wu, X., Ding, Y., Shao, F., Cao, Q., Jiang, Y., Li, X., Xu, Y., Zhao, Z., Xu, M., Lu, J., et al. (2026) · Cardiovascular Diabetology · doi:10.1186/s12933-026-03194-0
Alteration of bile acid metabolism in mice under thermoneutral conditions
Soma, H., Yoshida, R., & Ishizuka, S. (2026) · Steroids · doi:10.1016/j.steroids.2026.109794
Ecology and engineering to modify the bile acid output of a defined microbial communityPreprint
Zeng, X., Meng, X., Weakley, A. M., Jarrett, K. E., Higginbottom, S. K., Lopez, E. M., Cabrera, A. V., Gray, I. J., DeFelice, B. C., Terasaki, M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.23.727444
Ren, X., Zhou, S., & Li, Y. (2026) · Healthcare · doi:10.3390/healthcare14121712
Rui, L. I., Li-Yun, S. H. A., You-Guan, H. E. N. G., & Shen, W.-Q. (2026) · Shengming kexue · doi:10.3724/cbls.2026077
Clinical Relevance of Bile Acid and Bile Acid-Related Therapy in Liver Cirrhosis: A Review
Cao, G., Zhao, H., Lin, G., Chen, J., Gao, C., Méndez‐Sánchez, N., Gao, F., & Qi, X. (2026) · Advances in Therapy · doi:10.1007/s12325-026-03696-z
Gao, W., Shi, J., Xie, L., Xiao, P., Chen, W., Feng, Q., Gan, K.-X., Fu, G., Wu, J., Liu, W., et al. (2026) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2026.122328
Ramos, S. F., Fogelson, K. A., Muti, V. B., Aron, A. T., Salido, R. A., Richter, R. A., Mannochio-Russo, H., Hu, J., Hosseini, M., Loomba, R. S., et al. (2026) · mSystems · doi:10.1128/msystems.00720-26
Wang, W., Tang, Y., Wan, Z., Zhang, Z., Zheng, Z., Liu, H., Shu, Q., & Li, S. (2026) · Pharmacological Research · doi:10.1016/j.phrs.2026.108444
Kaplina, A., Bueverov, A. O., Ipatova, M. G., Kravchuk, Y. A., Peresada, O. A., Seliverstov, P. V., Serkova, M. Y., Sitkin, S. I., Яковенко, Э. П., Александровна, Б. Е., et al. (2026) · Almanac of Clinical Medicine · doi:10.18786/2072-0505-2026-54-017
Gut microbiota shaping fatty liver disease progression
Wysokińska, M., Mysza, M., Uryga, A., & Kolodziejczyk, A. A. (2026) · Life Science Alliance · doi:10.26508/lsa.202603756
Qin, Z., Juramt, D., Chen, Y., Li, Y., Wei, J., Yang, H., Chen, L., & Qiu, W. (2026) · Frontiers in Medicine · doi:10.3389/fmed.2026.1946657
Metabolic Dysfunction‐Associated Steatotic Liver Disease
Kanwal, F., & Wong, V. W. S. (2026) · Wiley eBooks · doi:10.1002/9781394360031.ch31
Crosstalk along the gut–liver axis in liver disease: Clinical and mechanistic aspects
Nakamoto, N., Okada, H., Bäckhed, F., Schnabl, B., & Hov, J. R. (2026) · Journal of Hepatology · doi:10.1016/j.jhep.2026.10.019
Chen, Y., Li, Y., Li, X., Xu, X., & Chen, S. (2026) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2026.1962509
Metadata
- Authors
- Puri, P., Daita, K., Joyce, A., Mirshahi, F., Santhekadur, P. K., Cazanave, S., Luketic, V. A., Siddiqui, M. S., Boyett, S., Min, H., Kumar, D. P., Kohli, R., Zhou, H., Hylemon, P. B., Contos, M. J., Idowu, M., & Sanyal, A. J.
- Affiliations
- Virginia Commonwealth University (US)
- Venebio (United States) (US)
- University of Southern California (US)
- Corresponding author
- Puri, Puneet
- ORCID
- Venue
- Hepatology
- Published
- 2017-12-23
- Volume
- 67
- Issue
- 2
- Pages
- 534-548
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- PMC
- PMC5764808
- OpenAlex
- W2735896722
- Cited by
- 426
- References
- 38
- Citations by year
- 2026: 34 · 2025: 52 · 2024: 59 · 2023: 42 · 2022: 55 · 2021: 69 · 2020: 40 · 2019: 39 · 2018: 31 · 2017: 4
- FWCI
- 24.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Bristol-Myers Squibb
- GlaxoSmithKline
- American Association for the Study of Liver Diseases
- Gilead Sciences
- National Institutes of Health (R01 DK 10596‐01, UL1TR000058)
- National Institute on Alcohol Abuse and Alcoholism (K23AA021179)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK105961, R01DK100314, T32DK007150, R01DK081410, P30DK048522)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Keywords
- nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, bile acids, chenodeoxycholic acid, cholic acid, taurocholate, liver fibrosis, steatosis, liver histopathology, NAFLD activity score, type 2 diabetes, hepatocyte ballooning, inflammation, cirrhosis risk, biomarkers
- MeSH terms
- Receptor, Farnesoid X-Activated, Adult, Aged, Bile Acids and Salts, Cross-Sectional Studies, Female, Humans, Liver Cirrhosis, Male, Middle Aged, Prospective Studies, Severity of Illness Index, Receptors, Cytoplasmic and Nuclear, Non-alcoholic Fatty Liver Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
