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MAFB as a novel regulator of human adipose tissue inflammation

Overview of attention for article published in Diabetologia, June 2015
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About this Attention Score

  • Good Attention Score compared to outputs of the same age (69th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (63rd percentile)

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2 X users
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1 patent

Citations

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34 Dimensions

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37 Mendeley
Title
MAFB as a novel regulator of human adipose tissue inflammation
Published in
Diabetologia, June 2015
DOI 10.1007/s00125-015-3673-x
Pubmed ID
Authors

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

Abstract

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

X Demographics

X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 3%
Unknown 36 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 16%
Researcher 6 16%
Student > Master 5 14%
Other 3 8%
Professor > Associate Professor 3 8%
Other 7 19%
Unknown 7 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 24%
Medicine and Dentistry 6 16%
Agricultural and Biological Sciences 5 14%
Immunology and Microbiology 4 11%
Sports and Recreations 2 5%
Other 3 8%
Unknown 8 22%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 January 2020.
All research outputs
#6,794,654
of 22,816,807 outputs
Outputs from Diabetologia
#2,662
of 5,036 outputs
Outputs of similar age
#78,465
of 263,249 outputs
Outputs of similar age from Diabetologia
#30
of 85 outputs
Altmetric has tracked 22,816,807 research outputs across all sources so far. This one has received more attention than most of these and is in the 69th percentile.
So far Altmetric has tracked 5,036 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 22.6. This one is in the 46th percentile – i.e., 46% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 263,249 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 69% of its contemporaries.
We're also able to compare this research output to 85 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 63% of its contemporaries.