Evidence map›Paper›PMID 27621190›Full record

ArticleMetabolism: clinical and experimental2016

Activin A and follistatin in patients with nonalcoholic fatty liver disease.

Stergios A Polyzos, Jannis Kountouras, Athanasios D Anastasilakis, Georgios Α Triantafyllou, Christos S Mantzoros

Open access · greenAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Follistatin Alleviates Hepatic Steatosis in NAFLD via the mTOR Dependent Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  15. Review
  16. Hepatokines as a Molecular Transducer of Exercise.Journal of clinical medicine · 2021
    Review
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  18. Observational
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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 2 countries.

Stergios A PolyzosDepartment of Medicine, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece. Electronic address: stergios@endo.gr.
Jannis KountourasDepartment of Medicine, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece.
Athanasios D AnastasilakisDepartment of Endocrinology, 424 General Military Hospital, Thessaloniki, Greece.
Georgios Α TriantafyllouDivision of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Christos S MantzorosDivision of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Aristotle University of Thessaloniki · GRBeth Israel Deaconess Medical Center · US424 General Military Hospital · GR

Funding

Leptin and Adipokine PhysiologyK24DK081913 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 2008 to 2020
$1.5M
NIDDK NIH HHS K24 DK081913
6 · The paper itself

Abstract

objectiveThere are limited data on the role of activin A and its binding protein, follistatin, in nonalcoholic fatty liver disease (NAFLD). The main aim was the evaluation of serum activin A and follistatin levels in patients with biopsy-proven NAFLD vs.

methodsThis was a case-control study. Fifteen patients with nonalcoholic simple steatosis (SS), 16 with steatohepatitis (NASH), and 52 (24 lean and 28 obese) controls were recruited. Activin A and follistatin were measured using ELISA.

resultsActivin A levels showed a trend towards progressive increase (p=0.010) from the controls (lean: 356±25, 95% CI 305-408; obese 360±20, 95% CI 320-401pg/ml) to SS (407±28, 95% CI 347-466pg/ml) and NASH patients (514±70 95% CI 364-664pg/ml); this association became non-significant after adjusting for adiposity. Follistatin was not different between groups (lean controls: 1.11±0.08, 95% CI 0.95-1.28; obese controls: 1.00±0.07, 95% CI 0.86-1.14; SS: 0.86±0.07, 95% CI 0.70-1.02; NASH: 1.14±0.09, 95% CI 0.90-1.37ng/ml; p=0.13). Within the NAFLD group of patients, follistatin was associated with NASH independently from activin A, gender and age, a relationship however likely reflecting the effect of adiposity.

conclusionsActivin A is higher in patients with NASH than both lean and obese controls. Future clinical studies are needed to confirm and expand these findings, whereas mechanistic studies exploring underlying mechanisms are also warranted.

Indexed as

ActivinsAdiposityAgingBiopsyBody Mass IndexCase-Control StudiesFatty LiverFemaleFollistatinHumansLiver Function TestsMaleMiddle AgedNon-alcoholic Fatty Liver DiseaseObesitySex Characteristicsactivin AActivinsFollistatinFST protein, humanActivin AFollistatinNonalcoholic fatty live diseaseNonalcoholic steatohepatitisSteatosis

Identifiers

PMID27621190
PMCPMC5022788
OpenAlexW2500667229

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.