Evidence map›Paper›PMID 27358174›Full record

ReviewHepatology (Baltimore, Md.)2017

Bile acids and nonalcoholic fatty liver disease: Molecular insights and therapeutic perspectives.

Juan P Arab, Saul J Karpen, Paul A Dawson, Marco Arrese, Michael Trauner

Open access · hybridAbstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 345 papers.

0numbers the graph read from it
0cells of the map it votes in
345citing papers in PubMed
21.3field-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

345 citing papers in PubMed, 598 citations in OpenAlex.

  1. Trial
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  9. Observational
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  11. The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026
    Review
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285 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

5 authors at 3 institutions in 3 countries.

Juan P ArabDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Saul J KarpenDivision of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Paul A DawsonDivision of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Marco ArreseDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Michael TraunerDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Emory University · USPontificia Universidad Católica de Chile · CLMedical University of Vienna · AT

Funding

ILEAL BILE ACID TRANSPORTER METABOLISM AND REGULATIONR01DK047987 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DAWSON, PAUL A · 2000 to 2021
$6.8M
MOLECULAR REGULATION OF HEPATIC TRANSPORTERSR01DK056239 · NIDDK · YALE UNIVERSITY · PI KARPEN, SAUL J. · 1999 to 2017
$4.8M
ILEAL BILE ACID TRANSPORTER METABOLISM AND REGULATIONR29DK047987 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DAWSON, PAUL A · 1994 to 1998
–
NIDDK NIH HHS R01 DK047987NIDDK NIH HHS R01 DK056239NIDDK NIH HHS R29 DK047987
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an important risk factor for both hepatic and cardiometabolic mortality. The rapidly increasing prevalence of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches to prevent disease progression to advanced fibrosis or cirrhosis and cancer. In recent years, bile acids have emerged as relevant signaling molecules that act at both hepatic and extrahepatic tissues to regulate lipid and carbohydrate metabolic pathways as well as energy homeostasis. Activation or modulation of bile acid receptors, such as the farnesoid X receptor and TGR5, and transporters, such as the ileal apical sodium-dependent bile acid transporter, appear to affect both insulin sensitivity and NAFLD/NASH pathogenesis at multiple levels, and these approaches hold promise as novel therapies. In the present review, we summarize current available data on the relationships of bile acids to NAFLD and the potential for therapeutically targeting bile-acid-related pathways to address this growing world-wide disease. (Hepatology 2017;65:350-362).

Indexed as

Bile Acids and SaltsEnergy MetabolismGlucoseHumansInflammationLipid MetabolismLiverMicrobiotaNon-alcoholic Fatty Liver DiseaseReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-CoupledSignal TransductionBile Acids and SaltsGlucoseGPBAR1 protein, humanReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-Coupled

Identifiers

PMID27358174
PMCPMC5191969
OpenAlexW2468692184

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.