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Cited by 64Effects and risks of endocrine disrupting chemicalsBirth, Development, and HealthToxic Organic Pollutants Impact

In vivo and in vitro bisphenol A exposure effects on adiposity

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Desai, M., Ferrini, M. G., Jellyman, J. K., Han, G., Ross, M. G.·2018·Journal of Developmental Origins of Health and Disease
DOI 10.1017/s2040174418000600PMC PMC6363869
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Abstract

In utero exposure to the ubiquitous plasticizer, bisphenol A (BPA) is associated with offspring obesity. As adipogenesis is a critical factor contributing to obesity, we determined the effects of in vivo maternal BPA and in vitro BPA exposure on newborn adipose tissue at the stem-cell level. For in vivo studies, female rats received BPA before and during pregnancy and lactation via drinking water, and offspring were studied for measures of adiposity signals. For in vitro BPA exposure, primary pre-adipocyte cell cultures from healthy newborns were utilized. We studied pre-adipocyte proliferative and differentiation effects of BPA and explored putative signal factors which partly explain adipose responses and underlying epigenetic mechanisms mediated by BPA. Maternal BPA-induced offspring adiposity, hypertrophic adipocytes and increased adipose tissue protein expression of pro-adipogenic and lipogenic factors. Consistent with in vivo data, in vitro BPA exposure induced a dose-dependent increase in pre-adipocyte proliferation and increased adipocyte lipid content. In vivo and in vitro BPA exposure promotes the proliferation and differentiation of adipocytes, contributing to an enhanced capacity for lipid storage. These findings reinforce the marked effects of BPA on adipogenesis and highlight the susceptibility of stem-cell populations during early life with long-term consequence on metabolic homeostasis.

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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 [106]

    The Results (Maternal BPA Effects on Offspring Phenotype; page not provided) report increased body fat in BPA-exposed males at 3 and 24 weeks, but no increase in females. The paper does not study phthalate exposure; phthalates appear only in a cited reference. Thus it supports a later-life adiposity effect of maternal BPA exposure, but not the claim that BPA and phthalate studies have consistently shown that effect. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Synthetic chemicals such as BPA and phalates are thought to promote obesity in children and adults by increasing adipogenesis.

    “These synthetic chemicals are thought to promote obesity in children and adults by increasing adipogenesis [105, 106].”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [106]

    The Discussion (page unavailable) reports increased fat accumulation in BPA-exposed rat offspring and increased adipogenic activity in BPA-exposed cells. It also notes an association between BPA exposure and adiposity in children. The paper does not establish that phthalates promote obesity through adipogenesis, or demonstrate that this mechanism promotes obesity in adult humans. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • 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].”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [106]

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Cited by

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Authors
Desai, M., Ferrini, M. G., Jellyman, J. K., Han, G., & Ross, M. G.
Affiliations
  • University of California, Los Angeles (US)
  • Charles R. Drew University of Medicine and Science (US)
  • The Lundquist Institute (US)
Corresponding author
Desai, M.
ORCID
Venue
Journal of Developmental Origins of Health and Disease
Publisher
Cambridge University Press (CUP)
Published
2018-08-29
Volume
9
Issue
6
Pages
678-687
ISSN
  • 2040-1744 (ISSN-L)
  • 2040-1752
DOI
10.1017/s2040174418000600
PMC
PMC6363869
OpenAlex
W2889492562
Cited by
64
References
4
Citations by year
2026: 5 · 2025: 4 · 2024: 13 · 2023: 8 · 2022: 12 · 2021: 9 · 2020: 8 · 2019: 4 · 2018: 1
FWCI
2.72
Type
journal article
Language
en
Open access
Licence
www.cambridge.org/core/terms (unspecified)
Locations
  • Journal of Developmental Origins of Health and Disease (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (UL1TR000124)
  • National Institute of Environmental Health Sciences (R21ES023112)
  • National Center for Advancing Translational Sciences
  • National Institute on Minority Health and Health Disparities (U54MD007598)
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
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Keywords
bisphenol A, offspring obesity, adipogenesis, adipose tissue, epigenetic mechanisms, plasticizers, developmental origins of health and disease, lipogenesis, adipocyte hypertrophy, fat deposition
MeSH terms
Bisphenol A Compounds, Adipose Tissue, Animals, Animals, Newborn, Benzhydryl Compounds, Cell Differentiation, Cells, Cultured, Disease Models, Animal, Estrogens, Non-Steroidal, Female, Humans, Male, Obesity, Phenols, Pregnancy, Rats, Sprague-Dawley, Adipocytes, Maternal Exposure, Cell Proliferation, Adiposity, Adipogenesis, Rats, Endocrine Disruptors, Mesenchymal Stem Cells, Primary Cell Culture

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