Evidence map›Paper›PMID 23506355›Full record

ArticleArchives of physiology and biochemistry2013

Prednisolone induces the Wnt signalling pathway in 3T3-L1 adipocytes.

Wilco W M Fleuren, Margot M L Linssen, Erik J M Toonen, Gerard C M van der Zon, Bruno Guigas, Jacob de Vlieg, Wim H A Dokter, D Margriet Ouwens, Wynand Alkema

Open access · bronzeAbstract read
In one paragraph

Article in Archives of physiology and biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

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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

9 authors at 6 institutions in 3 countries.

Wilco W M FleurenCDD, CMBI, NCMLS, Radboud University Medical Centre, Nijmegen, The Netherlands.
Margot M L Linssen
Erik J M Toonen
Gerard C M van der Zon
Bruno Guigas
Jacob de Vlieg
Wim H A Dokter
D Margriet Ouwens
Wynand Alkema
Leiden University Medical Center · NLRadboud University Medical Center · NLGhent University Hospital · BENetherlands eScience Center · NLRadboud University Nijmegen · NLSynthon (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synthetic glucocorticoids are potent anti-inflammatory drugs but show dose-dependent metabolic side effects such as the development of insulin resistance and obesity. The precise mechanisms involved in these glucocorticoid-induced side effects, and especially the participation of adipose tissue in this are not completely understood. We used a combination of transcriptomics, antibody arrays and bioinformatics approaches to characterize prednisolone-induced alterations in gene expression and adipokine secretion, which could underlie metabolic dysfunction in 3T3-L1 adipocytes. Several pathways, including cytokine signalling, Akt signalling, and Wnt signalling were found to be regulated at multiple levels, showing that these processes are targeted by prednisolone. These results suggest that mechanisms by which prednisolone induce insulin resistance include dysregulation of wnt signalling and immune response processes. These pathways may provide interesting targets for the development of improved glucocorticoids.

Indexed as

3T3-L1 CellsAdipocytesAdipokinesAnimalsDeoxyglucoseGene ExpressionGlucocorticoidsImmunityInsulinInsulin ResistanceMicePrednisoloneSignal TransductionTissue Array AnalysisTranscriptomeWnt Signaling PathwayAdipokinesDeoxyglucoseGlucocorticoidsInsulinPrednisolone

Identifiers

PMID23506355
PMCPMC3665230
OpenAlexW2091227895

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.