ArticlePloS one2016
Low-Dose Bisphenol-A Impairs Adipogenesis and Generates Dysfunctional 3T3-L1 Adipocytes.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 203 citations in OpenAlex.
- The Association between Bisphenol A Exposure and Obesity in Children-A Systematic Review with Meta-Analysis.International journal of environmental research and public health · 2019Pooled it
- Bisphenol A exposure and type 2 diabetes mellitus risk: a meta-analysis.BMC endocrine disorders · 2018Pooled it
- Emerging evidence for skeletal muscle as a target of BPA exposure.BMC endocrine disorders · 2026Review
- Identification and Validation of Biomarkers in Chronic Rhinosinusitis With Nasal Polyps and Study of Their Associated Mechanisms.World journal of otorhinolaryngology - head and neck surgery · 2025Article
- Liquid Crystal Monomers and Their Mixtures Alter Nuclear Receptor Signaling and Promote Adipogenesis In Vitro.Endocrinology · 2025Article
- Exploring the inhibitory effects ofFood science and biotechnology · 2025Article
- Consensus on the key characteristics of metabolism disruptors.Nature reviews. Endocrinology · 2025Review
- Article
- Research status of anti-obesogenic functional foods: mechanism of endocrine-disrupting chemicals and glucocorticoid receptor pathway.Food science and biotechnology · 2025Review
- Preventive role of Pastinaca sativa in mitigating metabolic dysfunction-associated steatotic liver disease via modulation of metabolic endotoxemia.NPJ science of food · 2025Article
- Analysis of bisphenol A-modulated expression of hypothalamic thyroid, estrogen, and peroxisome proliferator-activated receptors and concurrent mitochondrial dynamics following short-term exposure in mice.Current research in toxicology · 2025Article
- Genetic susceptibility to gestational diabetes and its mild modification by bisphenol A and thyroid-stimulating hormone: findings from a South Chinese pregnancy cohort.Frontiers in nutrition · 2025Article
- Microplastic Exposure and Its Dual Impact on Metabolic Syndrome and Pathways of Colorectal Carcinogenesis: A Systematic Review of Epidemiological, Experimental, and Mechanistic Evidence.Journal of toxicology · 2025Review
- 1,25‑Dihydroxyvitamin D3 mitigates the adipogenesis induced by bisphenol A in 3T3-L1 and hAMSC through miR-27-3p regulation.International journal of obesity (2005) · 2024Article
- Dietary bisphenols exposure as an influencing factor of body mass index.Environmental health : a global access science source · 2024Article
- Structural Studies on the Binding Mode of Bisphenols to PPARγ.Biomolecules · 2024Article
- Endocrine disrupting chemicals: gestational diabetes and beyond.Diabetology & metabolic syndrome · 2024Review
- Obesogens: a unifying theory for the global rise in obesity.International journal of obesity (2005) · 2024Review
- Metabolic effects of nuclear receptor activation in vivo after 28-day oral exposure to three endocrine-disrupting chemicals.Archives of toxicology · 2024Article
- Bombesin-like receptor 3 expression induced by bisphenol A is likely associated with reduced cell proliferation by inhibiting DNA synthesis and inducing inflammation in liver cells.Molecular biology reports · 2024Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Environmental endocrine disruptors (EDCs), including bisphenol-A (BPA), have been recently involved in obesity and diabetes by dysregulating adipose tissue function. Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. Therefore, 3T3-L1 pre-adipocytes were cultured for three weeks with BPA 1 nM to mimic human environmental exposure. We evaluated BPA effect on cell proliferation, differentiation, gene expression and adipocyte metabolic function. BPA significantly increased pre-adipocyte proliferation (p<0.01). In 3T3-L1 adipocytes differentiated in the presence of BPA, the expression of Peroxisome proliferator-activated receptor gamma (PPARγ), Fatty Acid Binding Protein 4/Adipocyte Protein 2 (FABP4/AP2) and CCAAT/enhancer binding protein (C/EBPα) was increased by 3.5, 1.5 and 3 folds, respectively. Mature adipocytes also showed a significant increase in lipid accumulation (p<0.05) and alterations of insulin action, with significant reduction in insulin-stimulated glucose utilization (p<0.001). Moreover, in mature adipocytes, mRNA levels of Leptin, interleukin-6 (IL6) and interferon-γ (IFNγ) were significantly increased (p<0.05). In conclusion, BPA prolonged exposure at low doses, consistent with those found in the environment, may affect adipocyte differentiation program, enhancing pre-adipocyte proliferation and anticipating the expression of the master genes involved in lipid/glucose metabolism. The resulting adipocytes are hypertrophic, with impaired insulin signaling, reduced glucose utilization and increased pro-inflammatory cytokine expression. Thus, these data supported the hypothesis that BPA exposure, during critical stages of adipose tissue development, may cause adipocyte metabolic dysfunction and inflammation, thereby increasing the risk of developing obesity-related diseases.
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Registered trials
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.