Evidence map›Paper›PMID 31571251›Full record

ArticleHepatology (Baltimore, Md.)2020

Probiotic Lactobacillus rhamnosus GG Prevents Liver Fibrosis Through Inhibiting Hepatic Bile Acid Synthesis and Enhancing Bile Acid Excretion in Mice.

Yunhuan Liu, Kefei Chen, Fengyuan Li, Zelin Gu, Qi Liu, Liqing He, Tuo Shao, Qing Song, Fenxia Zhu, Lihua Zhang and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 5 pooled it
10.8field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

193 citing papers in PubMed, 5 syntheses or guidelines pooled it, 340 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 2 countries.

Yunhuan LiuDepartment of Medicine, University of Louisville, Louisville, KY.ORCID 0000-0001-5456-5347
Kefei ChenDepartment of Medicine, University of Louisville, Louisville, KY.
Fengyuan LiDepartment of Medicine, University of Louisville, Louisville, KY.
Zelin GuDepartment of Medicine, University of Louisville, Louisville, KY.
Qi LiuDepartment of Medicine, University of Louisville, Louisville, KY.
Liqing HeDepartment of Chemistry, University of Louisville, Louisville, KY.
Tuo ShaoDepartment of Medicine, University of Louisville, Louisville, KY.
Qing SongDepartment of Medicine, University of Louisville, Louisville, KY.
Fenxia ZhuDepartment of Medicine, University of Louisville, Louisville, KY.
Lihua ZhangDepartment of Medicine, University of Louisville, Louisville, KY.
Mengwei JiangDepartment of Medicine, University of Louisville, Louisville, KY.
Yun ZhouDepartment of Medicine, University of Louisville, Louisville, KY.
Shirish BarveDepartment of Medicine, University of Louisville, Louisville, KY.
Xiang ZhangDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY.
Craig J McClainDepartment of Medicine, University of Louisville, Louisville, KY.
Wenke FengDepartment of Medicine, University of Louisville, Louisville, KY.
University of Louisville · USNanjing University of Chinese Medicine · CN

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2016 to 2025
$24.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI SHIRISH S BARVE · 2016 to 2026
$17.9M
Novel Therapies for Alcoholic HepatitisU01AA021893 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI MCCLAIN, CRAIG J., MCCULLOUGH, ARTHUR JOSEPH · 2012 to 2017
$6.0M
Mechanisms of Probiotics in Alcoholic Liver DiseaseR01AA023190 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2015 to 2024
$3.5M
Oxidized Metabolites of Linoleic Acid in Alcohol-induced Liver InjuryU01AA022489 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDSTEIN, ARIEL, MCCLAIN, CRAIG J. · 2014 to 2018
$1.7M
Mechanisms for alcohol induced gut barrier dysfunction in ALDR01AA023681 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2014 to 2018
$1.6M
Novel therapies in alcoholic hepatitis University of LouisvilleU01AA021901 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2012 to 2017
$1.5M
FGF21 and adipose lipolysis in alcoholic fatty liverR21AA022416 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2014 to 2015
$388k
Probiotics and HIF signaling in Alcoholic Liver DiseaseR21AA020848 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2013 to 2014
$376k
Dietary Fat and Alcoholic Liver DiseaseI01BX002996 · VA · LOUISVILLE VA MEDICAL MEDICAL CENTER · PI MCCLAIN, CRAIG J. · 2017 to 2020
–
BLRD VA I01 BX002996NIAAA NIH HHS P50 AA024337NIAAA NIH HHS P50AA024337NIAAA NIH HHS R01 AA023190NIAAA NIH HHS R01AA023190NIAAA NIH HHS R01 AA023681NIAAA NIH HHS R01AA023681NIAAA NIH HHS R21 AA020848NIAAA NIH HHS R21AA020848NIAAA NIH HHS R21 AA022416NIAAA NIH HHS U01 AA021893NIAAA NIH HHS U01AA021893-01NIAAA NIH HHS U01 AA021901NIAAA NIH HHS U01AA021901NIAAA NIH HHS U01 AA022489NIAAA NIH HHS U01AA022489-01A1NIGMS NIH HHS P20 GM113226NIGMS NIH HHS P20GM113226VA 1I01BX002996
6 · The paper itself

Abstract

BACKGROUND AND

aimsCholestatic liver disease is characterized by gut dysbiosis and excessive toxic hepatic bile acids (BAs). Modification of gut microbiota and repression of BA synthesis are potential strategies for the treatment of cholestatic liver disease. The purpose of this study was to examine the effects and to understand the mechanisms of the probiotic Lactobacillus rhamnosus GG (LGG) on hepatic BA synthesis, liver injury, and fibrosis in bile duct ligation (BDL) and multidrug resistance protein 2 knockout (Mdr2 APPROACH AND

resultsGlobal and intestine-specific farnesoid X receptor (FXR) inhibitors were used to dissect the role of FXR. LGG treatment significantly attenuated liver inflammation, injury, and fibrosis with a significant reduction of hepatic BAs in BDL mice. Hepatic concentration of taurine-β-muricholic acid (T-βMCA), an FXR antagonist, was markedly increased in BDL mice and reduced in LGG-treated mice, while chenodeoxycholic acid, an FXR agonist, was decreased in BDL mice and normalized in LGG-treated mice. LGG treatment significantly increased the expression of serum and ileum fibroblast growth factor 15 (FGF-15) and subsequently reduced hepatic cholesterol 7α-hydroxylase and BA synthesis in BDL and Mdr2

conclusionLGG supplementation decreases hepatic BA by increasing intestinal FXR-FGF-15 signaling pathway-mediated suppression of BA de novo synthesis and enhances BA excretion, which prevents excessive BA-induced liver injury and fibrosis in mice.

Indexed as

Bile Acids and SaltsCholestasisLiver CirrhosisReceptors, Cytoplasmic and NuclearAnimalsATP-Binding Cassette Sub-Family B Member 4ATP Binding Cassette Transporter, Subfamily BChenodeoxycholic AcidCholic AcidsFibroblast Growth FactorsGastrointestinal MicrobiomeHumansIntestinesLacticaseibacillus rhamnosusMiceMice, KnockoutATP-Binding Cassette Sub-Family B Member 4ATP Binding Cassette Transporter, Subfamily BBile Acids and SaltsChenodeoxycholic AcidCholic Acidsfibroblast growth factor 15, mouseFibroblast Growth Factorsmuricholic acidReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclear

Identifiers

PMID31571251
PMCPMC7317518
OpenAlexW2978988403

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

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.