Evidence map›Paper›PMID 25068083›Full record

ArticleAdipocyte2014

Bisphenol A increases aP2 expression in 3T3L1 by enhancing the transcriptional activity of nuclear receptors at the promoter.

Ella Atlas, Louise Pope, Mike G Wade, Alice Kawata, Adele Boudreau, Jonathan G Boucher

Open access · goldAbstract read
In one paragraph

Article in Adipocyte, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 11% 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, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pollution, stress response, and obesity: A systematic review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Pooled it
  2. Pooled it
  3. Effect ofAnimal biotechnology · 2024
    Article
  4. Tetra methyl bisphenol F: another potential obesogen.International journal of obesity (2005) · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Potential Mechanisms of Bisphenol A (BPA) Contributing to Human Disease.International journal of molecular sciences · 2020
    Review
  17. Bisphenol A enhances adipogenic signaling pathways in human mesenchymal stem cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2020
    Article
  18. Article
  19. Review
  20. Obesogenic Endocrine Disrupting Chemicals: Identifying Knowledge Gaps.Trends in endocrinology and metabolism: TEM · 2018
    Review
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

6 authors at 1 institution in 1 country.

Ella AtlasHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Louise PopeHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Mike G WadeHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Alice KawataHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Adele BoudreauHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Jonathan G BoucherHealth Canada; Environmental Health Science and Research Bureau; Ottawa, ON Canada.
Health Canada · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental pollutants, such as bisphenol A (BPA), have the potential to affect the differentiation processes and the biology of the adipose tissue. The 3T3-L1 model is one of the murine cell models used extensively for the investigation of the molecular events that govern the differentiation of adipocytes from a committed preadipocyte to a mature, lipid laden adipocyte. Most of the studies investigating the effects of BPA on preadipocyte differentiation have investigated the effects of this chemical in the presence of an optimal differentiation cocktail containing high concentrations of the synthetic glucocorticoid dexamethasone, conditions that result in 90% to 100% of differentiated adipocytes. Our studies employed the 3T3-L1 cell model in the absence of exogenous glucocorticoids. We show that BPA is able to increase the differentiation of the 3T3-L1 cells under these conditions. Furthermore, the effect of BPA was observed in the absence of the synthetic glucocorticoid (dexamethasone), a hormone known to be required for the differentiation of the 3T3-L1 cells. In addition, BPA upregulated the mRNA expression and protein levels of the terminal marker of adipogenesis the fatty acid binding protein (aP2) in these cells. Interestingly, the known modulators of adipogenesis such as the peroxisome proliferator-activated receptor (PPAR) γ or CCAAT enhancer binding protein (C/EBP) α were not elevated at the mRNA or protein level in response to BPA. Furthermore, BPA upregulated the expression levels of the marker of adipogenesis aP2, through an effect on the transcriptional activity of C/EBPδ and the glucocorticoid receptor (GR) at its promoter.

Indexed as

adipocyte differentiationadipogenesisaP2bisphenol AC/EBPδdifferentiationglucocorticoid receptorGRtranscription

Identifiers

PMID25068083
PMCPMC4110093
OpenAlexW2024210294

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.