Evidence map›Paper›PMID 26138654›Full record

ArticleDigestive diseases and sciences2015

Altered Bile Acid Metabolome in Patients with Nonalcoholic Steatohepatitis.

Brian C Ferslew, Guoxiang Xie, Curtis K Johnston, Mingming Su, Paul W Stewart, Wei Jia, Kim L R Brouwer, A Sidney Barritt

Registry-linked trialOpen access · greenAbstract readComparative Study
In one paragraph

Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03717883 (Endogenous Molecule Profiling in Subjects With Autosomal Dominant Polycystic Kidney Disease), which is not on this map. Cited by 193 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 4 pooled it
15.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

NCT03717883 completednot on this mapstarted 2018, after this paper: background citation

Endogenous Molecule Profiling in Subjects With Autosomal Dominant Polycystic Kidney Disease (ADPKD)

TypeobservationalSponsorUniversity of North Carolina, Chapel HillRan2018 to 2020Enrolled24ConditionsADPKD, Autosomal Dominant Polycystic Kidney Disease, Renal Disease
3 · Its place in the literature

Who cites it

193 citing papers in PubMed, 4 syntheses or guidelines pooled it, 327 citations in OpenAlex.

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133 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Brian C FerslewDivision of Pharmacotherapy and Experimental Therapeutics, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Kerr Hall, CB #7569, Chapel Hill, NC, 27599, USA. bferslew@theravance.com.
Guoxiang XieMetabolomics Shared Resource, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA. GXie@cc.hawaii.edu.
Curtis K JohnstonDivision of Pharmacotherapy and Experimental Therapeutics, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Kerr Hall, CB #7569, Chapel Hill, NC, 27599, USA. curtis.k.johnston@gmail.com.
Mingming SuMetabolomics Shared Resource, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA. MSu@cc.hawaii.edu.
Paul W StewartDepartment of Biostatistics, UNC Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 3105G McGavran-Greenberg Hall, Chapel Hill, NC, 27599, USA. Paul_Stewart@unc.edu.
Wei JiaMetabolomics Shared Resource, University of Hawaii Cancer Center, 701 Ilalo Street, Honolulu, HI, 96813, USA. WJia@cc.hawaii.edu.
Kim L R BrouwerDivision of Pharmacotherapy and Experimental Therapeutics, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Kerr Hall, CB #7569, Chapel Hill, NC, 27599, USA. kbrouwer@unc.edu.
A Sidney BarrittDivision of Gastroenterology and Hepatology, UNC School of Medicine, University of North Carolina at Chapel Hill, 8004 Burnett Womack, CB #7584, Chapel Hill, NC, 27599-7584, USA. sid_barritt@med.unc.edu.
University of North Carolina at Chapel Hill · USUniversity of Hawaii Cancer CenterUniversity of Hawaiʻi at Mānoa · US

Funding

University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI Xin Chen · 1996 to 2026
$56.2M
Re-Entry Supplement: Investigation of Oral Microbial Enzymes for the Detection and Treatment of Periodontal DiseaseUL1TR002489 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUSE, JOHN BERNARD, SHAHEEN, NICHOLAS J · 2018 to 2022
$48.6M
North Carolina Translational & Clinical Sciences Institute (NC TraCS)UL1TR001111 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUSE, JOHN BERNARD, CAREY, TIMOTHY S · 2013 to 2017
$43.9M
ALTERED HEPATIC DISPOSITION OF ANIONIC DRUGS-MECHANISMSR01GM041935 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BROUWER, KIM L.R. · 1997 to 2016
$6.5M
North Carolina Translational & Clinical Sciences Institute (NC TraCS)TL1TR001110 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUSE, JOHN BERNARD, CAREY, TIMOTHY S · 2013 to 2017
$489k
NCATS NIH HHS 1UL1TR001111NCATS NIH HHS TL1 TR001110NCATS NIH HHS UL1 TR001111NCATS NIH HHS UL1 TR002489NCI NIH HHS P30 CA071789NIGMS NIH HHS R01 GM041935
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe prevalence of nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) is increasing at an alarming rate. The role of bile acids in the development and progression of NAFLD to NASH and cirrhosis is poorly understood. This study aimed to quantify the bile acid metabolome in healthy subjects and patients with non-cirrhotic NASH under fasting conditions and after a standardized meal.

methodsLiquid chromatography tandem mass spectroscopy was used to quantify 30 serum and 16 urinary bile acids from 15 healthy volunteers and 7 patients with biopsy-confirmed NASH. Bile acid concentrations were measured at two fasting and four post-prandial time points following a high-fat meal to induce gallbladder contraction and bile acid reabsorption from the intestine.

resultsPatients with NASH had significantly higher total serum bile acid concentrations than healthy subjects under fasting conditions (2.2- to 2.4-fold increase in NASH; NASH 2595-3549 µM and healthy 1171-1458 µM) and at all post-prandial time points (1.7- to 2.2-fold increase in NASH; NASH 4444-5898 µM and healthy 2634-2829 µM). These changes were driven by increased taurine- and glycine-conjugated primary and secondary bile acids. Patients with NASH exhibited greater variability in their fasting and post-prandial bile acid profile.

conclusionsResults indicate that patients with NASH have higher fasting and post-prandial exposure to bile acids, including the more hydrophobic and cytotoxic secondary species. Increased bile acid exposure may be involved in liver injury and the pathogenesis of NAFLD and NASH.

Indexed as

MetabolomicsAdultBile Acids and SaltsBiomarkersCase-Control StudiesChromatography, LiquidDiscriminant AnalysisFastingFemaleHumansLeast-Squares AnalysisMaleMiddle AgedNon-alcoholic Fatty Liver DiseasePostprandial PeriodTandem Mass SpectrometryBile Acids and SaltsBiomarkersBile acid metabolomeBile acidsEnterohepatic recirculationNonalcoholic steatohepatitis

Identifiers

PMID26138654
PMCPMC4864493
OpenAlexW774501851

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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.