Evidence map›Paper›PMID 24966608›Full record

ReviewWorld journal of gastroenterology2014

Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease.

Kouichi Miura, Hirohide Ohnishi

Registry-linked trialOpen access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02526732 (Influence of Hepatic Inflammation and Hepatocellular Apoptosis on Physical Performance and Training Effect in Patients With Non - Alcoholic Steatohepatitis), which is not on this map. Cited by 181 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 1 pooled it
10.5field-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.

NCT02526732 nacompletednot on this mapstarted 2015, after this paper: background citation

Influence of Hepatic Inflammation and Hepatocellular Apoptosis on Physical Performance and Training Effect in Patients With Non - Alcoholic Steatohepatitis

TypeinterventionalSponsorPriv.-Doz. Dr. J. SchattenbergRan2015 to 2017Enrolled44ConditionsNon-alcoholic Fatty Liver DiseaseArmsindividual training program
3 · Its place in the literature

Who cites it

181 citing papers in PubMed, 1 synthesis or guideline pooled it, 352 citations in OpenAlex.

  1. Pooled it
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  15. Role of serum endotoxin, FGF19, TLR2, TNF-α, IL-12 and IL-10 in NAFLD-associated T2DM pathogenesis: Insights into Th1 bias and protective mechanisms.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2025
    Article
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121 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

2 authors at 1 institution in 1 country.

Kouichi MiuraKouichi Miura, Hirohide Ohnishi, Department of Gastroenterology, Akita University Graduate School of Medicine, Akita 010-8543, Japan.
Hirohide OhnishiKouichi Miura, Hirohide Ohnishi, Department of Gastroenterology, Akita University Graduate School of Medicine, Akita 010-8543, Japan.
Akita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging data have shown a close association between compositional changes in gut microbiota and the development of nonalcoholic fatty liver disease (NAFLD). The change in gut microbiota may alter nutritional absorption and storage. In addition, gut microbiota are a source of Toll-like receptor (TLR) ligands, and their compositional change can also increase the amount of TLR ligands delivered to the liver. TLR ligands can stimulate liver cells to produce proinflammatory cytokines. Therefore, the gut-liver axis has attracted much interest, particularly regarding the pathogenesis of NAFLD. The abundance of the major gut microbiota, including Firmicutes and Bacteroidetes, has been considered a potential underlying mechanism of obesity and NAFLD, but the role of these microbiota in NAFLD remains unknown. Several reports have demonstrated that certain gut microbiota are associated with the development of obesity and NAFLD. For instance, a decrease in Akkermansia muciniphila causes a thinner intestinal mucus layer and promotes gut permeability, which allows the leakage of bacterial components. Interventions to increase Akkermansia muciniphila improve the metabolic parameters in obesity and NAFLD. In children, the levels of Escherichia were significantly increased in nonalcoholic steatohepatitis (NASH) compared with those in obese control. Escherichia can produce ethanol, which promotes gut permeability. Thus, normalization of gut microbiota using probiotics or prebiotics is a promising treatment option for NAFLD. In addition, TLR signaling in the liver is activated, and its downstream molecules, such as proinflammatory cytokines, are increased in NAFLD. To data, TLR2, TLR4, TLR5, and TLR9 have been shown to be associated with the pathogenesis of NAFLD. Therefore, gut microbiota and TLRs are targets for NAFLD treatment.

Indexed as

AnimalsBacteriaBacterial TranslocationCytokinesHost-Pathogen InteractionsHumansImmunologic FactorsInflammation MediatorsIntestinal MucosaIntestinesLipid MetabolismLiverNon-alcoholic Fatty Liver DiseasePediatric ObesityPermeabilityProbioticsCytokinesImmunologic FactorsInflammation MediatorsToll-Like ReceptorsGut microbiotaNonalcoholic fatty liver diseaseNonalcoholic steatohepatitisPrebioticsProbioticsToll-like receptor

Identifiers

PMID24966608
PMCPMC4064083
OpenAlexW2013178634

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.