Environmental Endocrine Disruptors Promote Adipogenesis in the 3T3‐L1 Cell Line through Glucocorticoid Receptor Activation
Open accessAbstract
The burgeoning obesity and diabetes epidemics threaten health worldwide, yet the molecular mechanisms underlying these phenomena are incompletely understood. Recently, attention has focused on the potential contributions of environmental pollutants that act as endocrine disrupting chemicals (EDCs) in the pathogenesis of metabolic diseases. Because glucocorticoid signaling is central to adipocyte differentiation, the ability of EDCs to stimulate the glucocorticoid receptor (GR) and drive adipogenesis was assessed in the 3T3‐L1 cell line. Various EDCs were screened for glucocorticoid‐like activity using a luciferase reporter construct, and four (bisphenol A (BPA), dicyclohexyl phthalate (DCHP), endrin, and tolylfluanid (TF)) were shown to significantly stimulate GR without significant activation of the peroxisome proliferator‐activated receptor‐γ. 3T3‐L1 preadipocytes were then treated with EDCs and a weak differentiation cocktail containing dehydrocorticosterone (DHC) in place of the synthetic dexamethasone. The capacity of these compounds to promote adipogenesis was assessed by quantitative oil red O staining and immunoblotting for adipocyte‐specific proteins. The four EDCs increased lipid accumulation in the differentiating adipocytes and also upregulated the expression of adipocytic proteins. Interestingly, proadipogenic effects were observed at picomolar concentrations for several of the EDCs. Because there was no detectable adipogenesis when the preadipocytes were treated with compounds alone, the EDCs are likely promoting adipocyte differentiation by synergizing with agents present in the differentiation cocktail. Thus, EDCs are able to promote adipogenesis through the activation of the GR, further implicating these compounds in the rising rates of obesity and diabetes.
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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 [105]
The Abstract reports that BPA and dicyclohexyl phthalate increased adipogenesis in 3T3-L1 cells, and the Introduction describes a hypothesized link between synthetic chemicals and obesity. The paper does not establish that this mechanism promotes obesity in children or adults; its direct experiments were in cells, and the human evidence it discusses is correlational. No page numbers are available in our copy. (LLM, conf=0.87)
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- Authors
- Sargis, R. M., Johnson, D. N., Choudhury, R. A., & Brady, M. J.
- Affiliations
- University of Chicago (US)
- Corresponding author
- Brady, Matthew J.
- Venue
- Obesity
- Publisher
- Wiley
- Published
- 2010-07
- Volume
- 18
- Issue
- 7
- Pages
- 1283-1288
- ISSN
- 1930-7381 (ISSN-L)
- 1930-739X
- PMC
- PMC3957336
- OpenAlex
- W2036188881
- Cited by
- 305
- References
- 42
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 19 · 2023: 12 · 2022: 20 · 2021: 17 · 2020: 21 · 2019: 25 · 2018: 22 · 2017: 29 · 2016: 24 · 2015: 15 · 2014: 27 · 2013: 17 · 2012: 13
- FWCI
- 8.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Obesity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1f31es017391-01)
- National Institute of Environmental Health Sciences (F32ES017391, F31 ES017391, F32ES017397)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- endocrine disruptors, adipogenesis, glucocorticoid receptor, 3T3-L1 preadipocytes, bisphenol A, dicyclohexyl phthalate, endrin, tolylfluanid, lipid accumulation, diabetes mellitus, metabolic disorders, PPARγ
- MeSH terms
- Bisphenol A Compounds, Animals, Benzhydryl Compounds, Blood Proteins, Cell Differentiation, Cell Nucleus, Endocrine System, Endrin, Environment, Estrogens, Non-Steroidal, Genetic Testing, Glucocorticoids, Luciferases, Obesity, Phenols, Phthalic Acids, Prednisone, Receptors, Glucocorticoid, Stem Cells, Adipocytes, Genes, Reporter, 3T3-L1 Cells, Adipogenesis, Lipid Metabolism, Mice
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