Evidence map›Paper›PMID 28442273›Full record

ReviewMolecular aspects of medicine2017

The role of bile acids in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

Monica D Chow, Yi-Horng Lee, Grace L Guo

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 143 citations in OpenAlex.

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  17. Characterization of individual bile acids in vivo utilizing a novel low bile acid mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
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  19. Article
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6 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

3 authors at 1 institution in 1 country.

Monica D ChowDepartment of Surgery, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Yi-Horng LeeDivision of Pediatric Surgery, Department of Surgery, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Grace L GuoDepartment of Pharmacy and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, USA. Electronic address: guo@eohsi.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

Gut bile acids, Fxr, & Fgf15 in total parenteral nutrition-associated cholestasisR01GM104037 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI GUO, GRACE L · 2013 to 2016
$1.1M
FXR, nuclear receptors, and transcriptional regulation of liver homeostasisR56DK090036 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GUO, GRACE L · 2011 to 2011
$328k
NIDDK NIH HHS R56 DK090036NIGMS NIH HHS R01 GM104037
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease is growing in prevalence worldwide. It is marked by the presence of macrosteatosis on liver histology but is often clinically asymptomatic. However, it can progress into nonalcoholic steatohepatitis which is a more severe form of liver disease characterized by inflammation and fibrosis. Further progression leads to cirrhosis, which predisposes patients to hepatocellular carcinoma or liver failure. The mechanism by which simple steatosis progresses to steatohepatitis is not entirely clear. However, multiple pathways have been proposed. A common link amongst many of these pathways is disruption of the homeostasis of bile acids. Other than aiding in the absorption of lipids and lipid-soluble vitamins, bile acids act as ligands. For example, they bind to farnesoid X receptor, which is critically involved in many of the pathways responsible for maintaining bile acid, glucose, and lipid homeostasis. Alterations to these pathways can lead to dysregulation of energy balance and increased inflammation and fibrosis. Repeated insults over time may be the key to development of steatohepatitis. For this reason, current drug therapies target aspects of these pathways to try to reduce and halt inflammation and fibrosis. This review will focus on the role of bile acids in these various pathways and how changes in these pathways may result in steatohepatitis. While there is no approved pharmaceutical treatment for either hepatic steatosis or steatohepatitis, this review will also touch upon the multitude of potential therapies.

Indexed as

AzepinesBile Acids and SaltsCarcinoma, HepatocellularDisease ProgressionEnergy MetabolismGene Expression RegulationGlucoseHumansIndolesIsoxazolesLiverLiver CirrhosisLiver NeoplasmsNon-alcoholic Fatty Liver DiseasePregnane X ReceptorReceptor, Farnesoid X-Activated6-ethyl-24-norcholane-3,7,23-triol-23 sulfateAzepinesBile Acids and SaltsGlucoseGPBAR1 protein, humanGW 4064IndolesIsoxazolesPregnane X ReceptorReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-CoupledReceptors, SteroidWAY-362450Bile acidsEnterohepatic circulationFarnesoid X receptor (FXR)Gut-liver crosstalkNonalcoholic fatty liver disease (NAFLD)Nonalcoholic steatohepatitis (NASH)

Identifiers

PMID28442273
PMCPMC5812256
OpenAlexW2610304225

What OpenQuestion holds

Textmetadata
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.