Evidence map›Paper›PMID 25167060›Full record

ArticlePLoS computational biology2014

Possible role of interleukin-1β in type 2 diabetes onset and implications for anti-inflammatory therapy strategies.

Gang Zhao, Gitanjali Dharmadhikari, Kathrin Maedler, Michael Meyer-Hermann

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Role of Interleukins in Type 1 and Type 2 Diabetes.Diagnostics (Basel, Switzerland) · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Assessment of resveratrol on diabetes of zebrafish (Journal of diabetes and metabolic disorders · 2022
    Article
  15. Article
  16. Review
  17. Epigenetic Links between Microbiota and Gestational Diabetes.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  20. Frontiers in endocrinology · 2022
    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

4 authors at 2 institutions in 1 country.

Gang ZhaoDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Gitanjali DharmadhikariCentre for Biomolecular Interactions Bremen, University of Bremen, Bremen, Germany.
Kathrin MaedlerCentre for Biomolecular Interactions Bremen, University of Bremen, Bremen, Germany.
Michael Meyer-HermannDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany; Institute of Biochemistry, Biotechnology and Bioinformatics, Technische Universität Braunschweig, Braunschweig, Germany.
Helmholtz Centre for Infection Research · DEUniversity of Bremen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence of a role of chronic inflammation in type 2 diabetes progression has led to the development of therapies targeting the immune system. We develop a model of interleukin-1β dynamics in order to explain principles of disease onset. The parameters in the model are derived from in vitro experiments and patient data. In the framework of this model, an IL-1β switch is sufficient and necessary to account for type 2 diabetes onset. The model suggests that treatments targeting glucose bear the potential of stopping progression from pre-diabetes to overt type 2 diabetes. However, once in overt type 2 diabetes, these treatments have to be complemented by adjuvant anti-inflammatory therapies in order to stop or decelerate disease progression. Moreover, the model suggests that while glucose-lowering therapy needs to be continued all the way, dose and duration of the anti-inflammatory therapy needs to be specifically controlled. The model proposes a framework for the discussion of clinical trial outcomes.

Indexed as

Diabetes Mellitus, Type 2InflammationModels, ImmunologicalAnti-Inflammatory AgentsBlood GlucoseHumansHypoglycemic AgentsInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinAnti-Inflammatory AgentsBlood GlucoseHypoglycemic AgentsInterleukin-1betaInterleukin 1 Receptor Antagonist Protein

Identifiers

PMID25167060
PMCPMC4148195
OpenAlexW2043018206

What Socratic 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 Socratic graph.