Cited by 467Effects and risks of endocrine disrupting chemicalsBirth, Development, and HealthPeroxisome Proliferator-Activated Receptors

Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat

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Somm, Emmanuel, Schwitzgebel, Valérie M., Toulotte, Audrey, Cederroth, Christopher R., Combescure, Christophe, Nef, Serge, Aubert, Michel L., Hüppi, Petra S.·2009·Environmental Health Perspectives

Abstract

Background: The causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated. Objectives: The aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning. Methods: Pregnant Sprague-Dawley rats had access to drinking water containing 1 mg/L BPA from day 6 of gestation through the end of lactation. Pups were weaned on postnatal day (PND) 21. At that time, we investigated perigonadal adipose tissue of pups (weight, histology, gene expression). For the remaining animals, we recorded body weight and food intake for animals on either standard chow or a high-fat diet. Results: Gestational exposure to BPA did not alter the sex ratio or litter size at birth. On PND1, the weight of male and female BPA-exposed pups was increased. On PND21, body weight was increased only in females, in which parametrial white adipose tissue (pWAT) weight was increased about 3-fold. This excess of pWAT was associated with adipocyte hypertrophy and overexpression of lipogenic genes such as C/EBP-α (CAAT enhancer binding protein alpha), PPAR-γ (peroxisome proliferator-activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), LPL (lipoprotein lipase), FAS (fatty acid synthase), and SCD-1 (stearoyl-CoA desaturase 1). In addition, gene expression of SREBP-1C, FAS, and ACC (acetyl-CoA carboxylase) was also increased in liver from BPA-exposed females at PND21, without a change in circulating lipids and glucose. After weaning, perinatal BPA exposure predisposed to overweight in a sex- and diet-dependent manner. We observed no change in food intake due to perinatal BPA exposure in rats on either standard chow or a high-fat diet. Conclusions: Perinatal exposure to a low dose of BPA increased adipogenesis in females at weaning. Adult body weight may be programmed during early life, leading to changes dependent on the sex and the nutritional status. Although further studies are required to understand the mechanisms of BPA action in early life, these results are particularly important with regard to the increasing prevalence of childhood obesity and the context-dependent action of endocrine disruptors.

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  • Animal studies of BPA and phalate exposure in utero have consistently shown increased offspring adiposity in later life.

    “Animal studies of BPA and phalate exposure in utero have consistently shown to increase offspring adiposity in later life (Table 5 and [106, 110–112]).”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [110]

    The Results (Body weight and fat pad weights at weaning) report increased fat-pad weight in BPA-exposed female rat pups, and the Results (Postweaning body weight) report greater later body weight in females and in males on a high-fat diet. The paper does not report later-life adiposity measurements or phthalate exposure. Its Discussion also cites studies finding no change or reduced body weight, so it does not support the claim that animal studies have consistently found increased adiposity. (LLM, conf=0.90)

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  • BPA and phalates have been shown to exert sex-dependent impacts on offspring adiposity.

    “Likely due to their endocrine disrupting effects, BPA and phalates have been shown to exert sex-dependent impacts on offspring adiposity [106, 110].”

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Authors
Somm, E., Schwitzgebel, V. M., Toulotte, A., Cederroth, C. R., Combescure, C., Nef, S., Aubert, M. L., & Hüppi, P. S.
Affiliations
  • University of Geneva (CH)
  • University Hospital of Geneva (CH)
Corresponding author
Somm, Emmanuel
Venue
Environmental Health Perspectives
Published
2009-06-29
Volume
117
Issue
10
Pages
1549-1555
ISSN
  • 0091-6765 (ISSN-L)
  • 1552-9924
OpenAlex
W2024201289
Cited by
467
References
6
Citations by year
2026: 16 · 2025: 12 · 2024: 17 · 2023: 15 · 2022: 22 · 2021: 25 · 2020: 38 · 2019: 28 · 2018: 26 · 2017: 38 · 2016: 37 · 2015: 39 · 2014: 44 · 2013: 37 · 2012: 28
FWCI
17.28
Type
journal article
Language
en
Open access
Locations
  • Environmental Health Perspectives (publishedVersion, public-domain)
  • PubMed Central (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
bisphenol A, perinatal exposure, adipogenesis, endocrine disruptors, obesity, lipogenic gene expression, SREBP-1c, fatty acid synthase, hepatic gene expression, high-fat diet, sex differences, developmental programming, rats, weaning weight, adipocyte hypertrophy, dietary intake
MeSH terms
Bisphenol A Compounds, Adipose Tissue, Animals, Benzhydryl Compounds, Body Weight, Environmental Pollutants, Female, Litter Size, Liver, Male, Phenols, Pregnancy, Prenatal Exposure Delayed Effects, Sex Ratio, Weaning, Rats, Sprague-Dawley, Gene Expression Regulation, Developmental, Reverse Transcriptase Polymerase Chain Reaction, CCAAT-Enhancer-Binding Protein-alpha, PPAR gamma, Lipogenesis, Adipogenesis, Rats, Sterol Regulatory Element Binding Protein 1, In Vitro Techniques

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