Gut dysbiosis and impairment of immune system homeostasis in perinatally-exposed mice to Bisphenol A precede obese phenotype development
Open accessAbstract
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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These changes in offspring adiposity following BPA/phthalate exposure are associated with enhanced adipocyte size, infiltration of inflammatory leukocytes, and elevated expression of lipogenic markers like PPAR-γ and SREBP.
“In part, these changes are associated with enhanced adipocyte size, infiltration of inflammatory leukocytes, and elevated expression of lipogenic markers, like PPAR-γ and SREBP [113].”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [113]
The Results section reports increased gonadal white-adipose-tissue weight and a higher percentage of inflammatory M1 macrophages in BPA-exposed offspring at PND170. It does not report increased adipocyte size or elevated PPAR-γ or SREBP expression, and the study concerns BPA rather than phthalate exposure. The same Results passage says only IL-17 expression increased among the adipose-tissue genes tested. (LLM, conf=0.88)
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RetractedBISFENOL A: UMA AMEAÇA AOS HORMÔNIOS SEXUAIS
Pereira, S. C., de Oliveira, V. S., Moreira, R., Silva, F. R. M. B., Oliveira, C. P. F., & Alves, M. G. (2024) · Editora Reflexão Acadêmica eBooks · doi:10.51497/reflex.0000611
BISFENOL A: UMA AMEAÇA AOS HORMÔNIOS SEXUAIS
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OS PLÁSTICOS DO DIA A DIA: FTALATOS
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Emergentes ambientais: alerta à proteção da saúde
(2024) · Editora Reflexão Acadêmica eBooks · doi:10.51497/reflex.0000606
O MEIO AMBIENTE A SUA VOLTA E AS AMEAÇAS À SAÚDE: PIRIPROXIFENO PRÓS E CONTRAS
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- Authors
- Malaisé, Y., Menard, S., Cartier, C., Gaultier, E., Lasserre, F., Lencina, C., Harkat, C., Geoffre, N., Lakhal, L., Castan, I., Olier, M., Houdeau, E., & Guzylack-Piriou, L.
- Affiliations
- Université Toulouse III - Paul Sabatier (FR)
- ORCID
- Malaisé, Yann
- Venue
- Scientific Reports
- Published
- 2017-11-03
- Volume
- 7
- Issue
- 1
- Pages
- 14472-14472
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5670173
- OpenAlex
- W2767042225
- Cited by
- 107
- References
- 65
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 22 · 2023: 16 · 2022: 15 · 2021: 12 · 2020: 16 · 2019: 8 · 2018: 4 · 2017: 1
- FWCI
- 4.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-10-CESA-005, ANR-10-CESA-0005, ANR-10)
- Institut National de la Recherche Agronomique
- Agence Nationale de Sécurité Sanitaire de l’Alimentation, de l’Environnement et du Travail (EST-2015/1/026)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- bisphenol A, perinatal exposure, gut dysbiosis, gut microbiota, immune homeostasis, Th1/Th17 cells, lamina propria, IgA secretion, Bifidobacterium, M1 macrophages, white adipose tissue, insulin resistance, obesity, type 2 diabetes, low-grade inflammation, endocrine disruptors, metabolic disorders
- MeSH terms
- Gastrointestinal Microbiome, Bisphenol A Compounds, Animals, Animals, Newborn, Benzhydryl Compounds, Environmental Pollutants, Feces, Female, Glucose, Immunoglobulin A, Immune System, Inflammation, Longitudinal Studies, Male, Mice, Inbred C3H, Obesity, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Time Factors, Dysbiosis
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