ArticleScientific reports2017
Gut dysbiosis and impairment of immune system homeostasis in perinatally-exposed mice to Bisphenol A precede obese phenotype development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 102 citations in OpenAlex.
- The gut-brain axis mediates precocious puberty induced by environmentally relevant low-dose endocrine-disrupting chemical mixtures.Frontiers in endocrinology · 2025Pooled it
- Pooled it
- Agricultural chemicals and gut microbiota dysbiosis: implications for the pathogenesis of inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Obesity and obesity related disease in adulthood: the dark side of early life exposure to Environmental Chemical Disruptors.Journal of endocrinological investigation · 2025Review
- The relationship between gut microbiome and human diseases: mechanisms, predisposing factors and potential intervention.Frontiers in cellular and infection microbiology · 2025Review
- Unraveling the Role of the Human Gut Microbiome in Health and Diseases.Microorganisms · 2024Review
- Could environmental exposure and climate change Be a key factor in the rising incidence of early onset colorectal cancer?Heliyon · 2024Review
- Gestational bisphenol A exposure alters energy homeostasis and adult hypothalamic neurogenesis in female mice.Scientific reports · 2024Article
- Single-cell transcriptomics unveiled that early life BDE-99 exposure reprogrammed the gut-liver axis to promote a proinflammatory metabolic signature in male mice at late adulthood.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Evidence evaluated by European Food Safety Authority does not support lowering the temporary tolerable daily intake for bisphenol A.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Bisphenol A exposure affects specific gut taxa and drives microbiota dynamics in childhood obesity.mSystems · 2024Article
- Unmasking metabolic disruptors: The NEMESIS project's quest for Novel Biomarkers, Evidence on Adverse Effects, and Efficient Methodologies.Open research Europe · 2024Article
- Distinct gut flora profile induced by postnatal trans-fat diet in gestationally bisphenol A-exposed rats.PloS one · 2024Article
- Contribution of the microbiome for better phenotyping of people living with obesity.Reviews in endocrine & metabolic disorders · 2023Review
- The PCOS-NAFLD Multidisease Phenotype Occurred in Medaka Fish Four Generations after the Removal of Bisphenol A Exposure.Environmental science & technology · 2023Article
- The exposome and liver disease - how environmental factors affect liver health.Journal of hepatology · 2023Review
- A review on immunomodulatory effects of BPA analogues.Archives of toxicology · 2023Review
- New Evidence on BPA's Role in Adipose Tissue Development of Proinflammatory Processes and Its Relationship with Obesity.International journal of molecular sciences · 2023Review
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Microbial gut dysbiosis induced by xenobiotics in model organisms and the relevance of experimental criteria: a minireview.Gut microbiome (Cambridge, England) · 2023Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiology evidenced the Bisphenol A (BPA), a chemical found in daily consumer products, as an environmental contributor to obesity and type II diabetes (T2D) in Humans. However, the BPA-mediated effects supporting these metabolic disorders are still unknown. Knowing that obesity and T2D are associated with low-grade inflammation and gut dysbiosis, we performed a longitudinal study in mice to determine the sequential adverse effects of BPA on immune system and intestinal microbiota that could contribute to the development of metabolic disorders. We observed that perinatal exposure to BPA (50 µg/kg body weight/day) induced intestinal and systemic immune imbalances at PND45, through a decrease of Th1/Th17 cell frequencies in the lamina propria concomitant to an increase of splenic Th1/Th17 immune responses. These early effects are associated with an altered glucose sensitivity, a defect of IgA secretion into faeces and a fall of faecal bifidobacteria relative to control mice. Such BPA-mediated events precede infiltration of pro-inflammatory M1 macrophages in gonadal white adipose tissue appearing with ageing, together with a decreased insulin sensitivity and an increased weight gain. Our findings provide a better understanding of the sequential events provoked by perinatal exposure to BPA that could support metabolic disorder development in later life.
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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.