Evidence map›Paper›PMID 28962342›Full record

ArticleToxicology reports2015

Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice.

Johanna Bodin, Anette Kocbach Bølling, Anna Wendt, Lena Eliasson, Rune Becher, Frieke Kuper, Martinus Løvik, Unni Cecilie Nygaard

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-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

26 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  8. Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  9. Review
  10. Critical Overview on Endocrine Disruptors in Diabetes Mellitus.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Endocrine Disrupting Chemicals and Type 1 Diabetes.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
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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

8 authors at 3 institutions in 2 countries.

Johanna BodinDepartment of Food, Water and Cosmetics, Norwegian Institute of Public Health, Oslo, Norway.
Anette Kocbach BøllingDepartment of Air Pollution and Noise, Norwegian Institute of Public Health, Oslo, Norway.
Anna WendtLund University Diabetes Centre, Department of Clinical Sciences Malmö, Islet Cell Exocytosis, Lund University, CRC, Malmö, Sweden.
Lena EliassonLund University Diabetes Centre, Department of Clinical Sciences Malmö, Islet Cell Exocytosis, Lund University, CRC, Malmö, Sweden.
Rune BecherDepartment of Air Pollution and Noise, Norwegian Institute of Public Health, Oslo, Norway.
Frieke KuperTNO, Zeist, The Netherlands.
Martinus LøvikDepartment for Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University for Science and Technology, Trondheim, Norway.
Unni Cecilie NygaardDepartment of Food, Water and Cosmetics, Norwegian Institute of Public Health, Oslo, Norway.
Norwegian Institute of Public Health · NOLund University · SENorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune destruction of insulin producing pancreatic beta-cells due to a genetic predisposition and can be triggered by environmental factors. We have previously shown that bisphenol A (BPA) accelerates the spontaneous development of diabetes in non-obese diabetic (NOD) mice. Here, we hypothesized that oral exposure to a mixture of the endocrine disruptors BPA and phthalates, relevant for human exposure, would accelerate diabetes development compared to BPA alone. NOD mice were exposed to BPA (1 mg/l), a mixture of phthalates (DEHP 1 mg/l, DBP 0.2 mg/l, BBP 10 mg/l and DiBP 20 mg/l) or a combination of BPA and the phthalate mixture through drinking water from conception and throughout life. Previous observations that BPA exposure increased the prevalence of diabetes and insulitis and decreased the number of tissue resident macrophages in pancreas were confirmed, and extended by demonstrating that BPA exposure also impaired the phagocytic activity of peritoneal macrophages. None of these effects were observed after phthalate exposure alone. The phthalate exposure in combination with BPA seemed to dampen the BPA effects on macrophage number and function as well as diabetes development, but not insulitis development. Exposure to BPA alone or in combination with phthalates decreased cytokine release (TNFα, IL-6, IL-10, IFNγ, IL-4) from

Indexed as

BBP, butylbenzyl phthalateBisphenol ABPA, bisphenol ADBP, dibutyl phthalateDEHP, bis(2-ethylhexyl) benzene-1,2-dicarboxylateDiabetes mellitus type 1DiBP, diisobutyl phthalateImmunotoxicityInsulitisNOD micePhthalatesPrenatal exposure

Identifiers

PMID28962342
PMCPMC5598488
OpenAlexW2052110191

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.