Evidence map›Paper›PMID 28774887›Full record

ArticleGut2018

Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD.

Na Jiao, Susan S Baker, Adrian Chapa-Rodriguez, Wensheng Liu, Colleen A Nugent, Maria Tsompana, Lucy Mastrandrea, Michael J Buck, Robert D Baker, Robert J Genco and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Gut, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 421 papers.

0numbers the graph read from it
0cells of the map it votes in
421citing papers in PubMed
23.8field-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

421 citing papers in PubMed, 704 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Na JiaoDepartment of Bioinformatics, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Susan S BakerDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
Adrian Chapa-RodriguezDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
Wensheng LiuDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
Colleen A NugentDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
Maria TsompanaDepartment of Biochemistry and Center of Excellence in Bioinformatics and Life Sciences, The State University of New York at Buffalo, Buffalo, New York, USA.
Lucy MastrandreaDivision of Endocrinology, Department of Pediatrics, The State University of New York at Buffalo, Buffalo, New York, USA.
Michael J BuckGenome, Environment and Microbiome Community of Excellence, The State University of New York at Buffalo, Buffalo, New York, USA.
Robert D BakerDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
Robert J GencoGenome, Environment and Microbiome Community of Excellence, The State University of New York at Buffalo, Buffalo, New York, USA.
Ruixin ZhuDepartment of Bioinformatics, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Lixin ZhuDepartment of Pediatrics, Digestive Diseases and Nutrition Center, The State University of New York at Buffalo, Buffalo, New York, USA.
University at Buffalo, State University of New York · USTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBile acids are regulators of lipid and glucose metabolism, and modulate inflammation in the liver and other tissues. Primary bile acids such as cholic acid and chenodeoxycholic acid (CDCA) are produced in the liver, and converted into secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid by gut microbiota. Here we investigated the possible roles of bile acids in non-alcoholic fatty liver disease (NAFLD) pathogenesis and the impact of the gut microbiome on bile acid signalling in NAFLD.

designSerum bile acid levels and fibroblast growth factor 19 (FGF19), liver gene expression profiles and gut microbiome compositions were determined in patients with NAFLD, high-fat diet-fed rats and their controls.

resultsSerum concentrations of primary and secondary bile acids were increased in patients with NAFLD. In per cent, the farnesoid X receptor (FXR) antagonistic DCA was increased, while the agonistic CDCA was decreased in NAFLD. Increased mRNA expression for cytochrome P450 7A1, Na

conclusionsThe serum bile acid profile, the hepatic gene expression pattern and the gut microbiome composition consistently support an elevated bile acid production in NAFLD. The increased proportion of FXR antagonistic bile acid explains, at least in part, the suppression of hepatic FXR-mediated and FGFR4-mediated signalling. Our study suggests that future NAFLD intervention may target the components of FXR signalling, including the bile acid converting gut microbiome.

Indexed as

Bile Acids and SaltsNon-alcoholic Fatty Liver DiseaseAnimalsCholesterol 7-alpha-HydroxylaseDiet, High-FatFemaleFibroblast Growth FactorsGastrointestinal MicrobiomeGene Expression ProfilingHumansMaleMiddle AgedRatsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearSignal TransductionBile Acids and SaltsCholesterol 7-alpha-HydroxylaseCYP7A1 protein, humanFibroblast Growth FactorsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclearbile acidbile acid metabolismintestinal microbiologynonalcoholic steatohepatitis

Identifiers

PMID28774887
OpenAlexW2605955022

What OpenQuestion holds

Textmetadata
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.