Evidence map›Paper›PMID 27203081›Full record

ArticlePloS one2016

Bile Acids and Dysbiosis in Non-Alcoholic Fatty Liver Disease.

Marialena Mouzaki, Alice Y Wang, Robert Bandsma, Elena M Comelli, Bianca M Arendt, Ling Zhang, Scott Fung, Sandra E Fischer, Ian G McGilvray, Johane P Allard

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 2 pooled it
23.1field-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

224 citing papers in PubMed, 2 syntheses or guidelines pooled it, 381 citations in OpenAlex.

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  18. The complicated relationship between inflammation and metabolic dysfunction.Journal of diabetes and metabolic disorders · 2025
    Review
  19. Nutrients · 2025
    Article
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164 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

10 authors at 4 institutions in 1 country.

Marialena MouzakiDepartment of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, The Hospital for Sick Children, Toronto, ON, Canada.
Alice Y WangPhysiology and Experimental Medicine Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada.
Robert BandsmaDepartment of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, The Hospital for Sick Children, Toronto, ON, Canada.
Elena M ComelliDepartment of Nutritional Sciences, University of Toronto, Toronto, ON, Canada.
Bianca M ArendtToronto General Hospital, University Health Network, Toronto, ON, Canada.
Ling ZhangPhysiology and Experimental Medicine Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada.
Scott FungToronto General Hospital, University Health Network, Toronto, ON, Canada.
Sandra E FischerToronto General Hospital, University Health Network, Toronto, ON, Canada.
Ian G McGilvrayToronto General Hospital, University Health Network, Toronto, ON, Canada.
Johane P AllardToronto General Hospital, University Health Network, Toronto, ON, Canada.
Hospital for Sick Children · CAToronto General Hospital · CAUniversity Health Network · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsNon-alcoholic fatty liver disease (NAFLD) is characterized by dysbiosis. The bidirectional effects between intestinal microbiota (IM) and bile acids (BA) suggest that dysbiosis may be accompanied by an altered bile acid (BA) homeostasis, which in turn can contribute to the metabolic dysregulation seen in NAFLD. This study sought to examine BA homeostasis in patients with NAFLD and to relate that with IM data.

methodsThis was a prospective, cross-sectional study of adults with biopsy-confirmed NAFLD (non-alcoholic fatty liver: NAFL or non-alcoholic steatohepatitis: NASH) and healthy controls (HC). Clinical and laboratory data, stool samples and 7-day food records were collected. Fecal BA profiles, serum markers of BA synthesis 7-alpha-hydroxy-4-cholesten-3-one (C4) and intestinal BA signalling, as well as IM composition were assessed.

results53 subjects were included: 25 HC, 12 NAFL and 16 NASH. Levels of total fecal BA, cholic acid (CA), chenodeoxycholic acid (CDCA) and BA synthesis were higher in patients with NASH compared to HC (p<0.05 for all comparisons). The primary to secondary BA ratio was higher in NASH compared to HC (p = 0.004), but ratio of conjugated to unconjugated BAs was not different between the groups. Bacteroidetes and Clostridium leptum counts were decreased in in a subset of 16 patients with NASH compared to 25 HC, after adjusting for body mass index and weight-adjusted calorie intake (p = 0.028 and p = 0.030, respectively). C. leptum was positively correlated with fecal unconjugated lithocholic acid (LCA) (r = 0.526, p = 0.003) and inversely with unconjugated CA (r = -0.669, p<0.0001) and unconjugated CDCA (r = - 0.630, p<0.0001). FGF19 levels were not different between the groups (p = 0.114).

conclusionsIn adults with NAFLD, dysbiosis is associated with altered BA homeostasis, which renders them at increased risk of hepatic injury.

Indexed as

AdultBile Acids and SaltsCholestenonesCross-Sectional StudiesDysbiosisFecesFemaleFibroblast Growth FactorsHomeostasisHumansHydroxysteroid DehydrogenasesMaleMiddle AgedNon-alcoholic Fatty Liver DiseaseProspective Studies7 alpha-hydroxysteroid dehydrogenaseBile Acids and Saltscholest-4-en-3-oneCholestenonesFGF19 protein, humanFibroblast Growth FactorsHydroxysteroid Dehydrogenases

Identifiers

PMID27203081
PMCPMC4874546
OpenAlexW2396784827

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.