Evidence map›Paper›PMID 26115698›Full record

ArticleDiabetologia2015

MAFB as a novel regulator of human adipose tissue inflammation.

Annie M L Pettersson, Juan R Acosta, Christel Björk, Johan Krätzel, Britta Stenson, Lennart Blomqvist, Nathalie Viguerie, Dominique Langin, Peter Arner, Jurga Laurencikiene

Open access · bronzeAbstract read
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Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 30 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

10 authors at 3 institutions in 2 countries.

Annie M L PetterssonDepartment of Medicine Huddinge, Lipid laboratory, Karolinska Institutet, Novum, NVS D4, Hälsovägen 7, 14186, Stockholm, Sweden.
Juan R Acosta
Christel Björk
Johan Krätzel
Britta Stenson
Lennart Blomqvist
Nathalie Viguerie
Dominique Langin
Peter Arner
Jurga Laurencikiene
Karolinska Institutet · SEInstitut des Maladies Métaboliques et Cardiovasculaires · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisDysregulated expression of metabolic and inflammatory genes is a prominent consequence of obesity causing insulin resistance and type 2 diabetes. Finding causative factors is essential to understanding progression of these pathologies and discovering new therapeutic targets. The transcription factor V-maf musculoaponeurotic fibrosarcoma oncogene homologue B (MAFB) is highly expressed in human white adipose tissue (WAT). However, its role in the regulation of WAT function is elusive. We aimed to characterise MAFB expression and function in human WAT in the context of obesity and insulin resistance.

methodsMAFB mRNA expression was evaluated in human WAT from seven cohorts with large inter-individual variation in BMI and metabolic features. Insulin-induced adipocyte lipogenesis and lipolysis were measured and correlated with MAFB expression. MAFB regulation during adipogenesis and the effects of MAFB suppression in human adipocytes was investigated. MAFB regulation by TNF-α was examined in human primary adipocytes and THP-1 monocytes/macrophages.

resultsMAFB expression in human adipocytes is upregulated during adipogenesis, increases with BMI in WAT, correlates with adverse metabolic features and is decreased after weight loss. MAFB downregulation decreases proinflammatory gene expression in adipocytes and interferes with TNF-α effects. Interestingly, MAFB is differentially regulated by TNF-α in adipocytes (suppressed) and THP-1 cells (upregulated). Further, MAFB is primarily expressed in WAT macrophages/monocytes and its expression correlates with macrophage and inflammatory markers. CONCLUSIONS/

interpretationOur findings indicate that MAFB is a regulator and a marker of adipose tissue inflammation, a process that subsequently causes insulin resistance.

Indexed as

Gene Expression RegulationAdipocytesAdipose Tissue, WhiteBody Mass IndexCell DifferentiationCohort StudiesHumansInflammationInsulin ResistanceLipogenesisLipolysisMacrophagesMafB Transcription FactorMesenchymal Stem CellsMonocytesObesityMAFB protein, humanMafB Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID26115698
OpenAlexW841644910

What OpenQuestion holds

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Registered trials

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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.