Evidence map›Paper›PMID 25664838›Full record

ArticleNutrition & diabetes2015

Determining the association between adipokine expression in multiple tissues and phenotypic features of non-alcoholic fatty liver disease in obesity.

M G M Wolfs, N Gruben, S S Rensen, F J Verdam, J W Greve, A Driessen, C Wijmenga, W A Buurman, L Franke, L Scheja and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrition & diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Chemerin Isoforms and Activity in Obesity.International journal of molecular sciences · 2019
    Review
  19. Review
  20. Article
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

15 authors at 3 institutions in 2 countries.

M G M WolfsMolecular Genetics Section, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
N GrubenMolecular Genetics Section, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
S S RensenDepartment of General Surgery, Maastricht University Medical Center, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands.
F J VerdamDepartment of General Surgery, Maastricht University Medical Center, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands.
J W GreveDepartment of General Surgery, Maastricht University Medical Center, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands.
A Driessen1] Department of Pathology, Maastricht University Medical Centre, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands [2] Department of Pathology, University Hospital Antwerp, Edegem, Belgium.
C WijmengaDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
W A BuurmanSchool for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands.
L Franke1] Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London, UK.
L SchejaDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
D P Y KoonenMolecular Genetics Section, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
R Shiri-SverdlovDepartment of Molecular Genetics, Maastricht University, Maastricht, The Netherlands.
T W van Haeften1] Molecular Genetics Section, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] Department of Internal Medicine, University Medical Center Utrecht, Utrecht, The Netherlands.
M H HofkerMolecular Genetics Section, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
J FuDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Maastricht University · NLUniversity Medical Center Groningen · NLUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNon-alcoholic fatty liver disease (NAFLD) is an obesity-associated disease, and in obesity adipokines are believed to be involved in the development of NAFLD. However, it is still not clear whether adipokines in the liver and/or adipose tissues can be related to the development of specific characteristics of NAFLD, such as steatosis and inflammation. We aimed to address this question by simultaneously examining the adipokine expression in three tissue types in obese individuals.

methodsWe enrolled 93 severely obese individuals with NAFLD, varying from simple steatosis to severe non-alcoholic steatohepatitis. Their expression of 48 adipokines in the liver, visceral and subcutaneous adipose tissue (SAT) was correlated to their phenotypic features of NAFLD. We further determined whether the correlations were tissue specific and/or independent of covariates, including age, sex, obesity, insulin resistance and type 2 diabetes (T2D).

resultsThe expression of adipokines showed a liver- and adipose tissue-specific pattern. We identified that the expression of leptin, angiopoietin 2 (ANGPT2) and chemerin in visceral adipose tissue (VAT) was associated with different NAFLD features, including steatosis, ballooning, portal and lobular inflammation. In addition, the expression of tumor necrosis factor (TNF), plasminogen activator inhibitor type 1 (PAI-1), insulin-like growth factor 1 (somatomedin C) (IGF1) and chemokine (C-X-C motif) ligand 10 (CXCL10) in the liver tissue and the expression of interleukin 1 receptor antagonist (IL1RN) in both the liver and SAT were associated with NAFLD features. The correlations between ANGPT2 and CXCL10, and NAFLD features were dependent on insulin resistance and T2D, but for the other genes the correlation with at least one NAFLD feature remained significant after correcting for the covariates.

conclusionsOur results suggest that in obese individuals, VAT-derived leptin and chemerin, and hepatic expression of TNF, IGF1, IL1RN and PAI-1 are involved in the development of NAFLD features. Further, functional studies are warranted to establish a causal relationship.

Identifiers

PMID25664838
PMCPMC4338415
OpenAlexW2000532842

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.