Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors

Boucher, Jonathan; Ahmed, Shaimaa; Atlas, Ella

doi:10.1210/en.2015-1872

Cited by 116 publications

(72 citation statements)

References 50 publications

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“…12,18 They also have effects on peroxisome proliferator-activated receptor gamma (PPAR) signaling pathway, a main target of obesogens, to increase lipid accumulation and differentiation of preadipocytes into adipocytes. 19–21 In addition, BPF could affect adiponectin production and secretion. 18 Moreover, a recent study demonstrated that BPS exposure led to differentially expressed genes related to adipogenesis and lipid metabolism, and it had effects on adipose specific transcriptional changes earlier than BPA.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A substitutes and obesity in US adults: analysis of a population-based, cross-sectional study

Liu

Lehmler

Sun

et al. 2017

The Lancet Planetary Health

141

100

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Background Bisphenol F (BPF) and bisphenol S (BPS) are increasingly used to substitute bisphenol A (BPA), a widespread environmental endocrine disruptor and putative obesogen. However, studies on effects of BPF and BPS on obesity in humans are lacking. We examined the associations of BPA, BPF, and BPS exposure with obesity in U.S. adults. Methods We included 1,521 participants aged 20 years or older from a cross-sectional study, the National Health and Nutrition Examination Survey 2013–2014. Urinary BPA, BPF, and BPS concentrations were measured using on-line solid phase extraction coupled to high performance liquid chromatography and tandem mass spectrometry. We used body mass index and waist circumference to define general obesity and abdominal obesity, respectively. We used logistic regression with sample weights to estimate the odds ratios (ORs) of obesity and 95% confidence intervals. Findings Higher BPA, BPF, and BPS concentrations were observed in obese adults than non-obese adults. After adjustment for demographic, socioeconomic, lifestyle factors, and urinary creatinine concentrations, BPA, but not BPF or BPS, was significantly associated with obesity. The OR of general obesity was 1.78 (1.10–2.89) comparing the highest with lowest quartile of BPA, 1.02 (0.70–1.47) for BPF, and 1.22 (0.81–1.83) for BPS. The corresponding OR for abdominal obesity was 1.55 (1.04–2.32) for BPA, 1.05 (0.68–1.63) for BPF, and 1.16 (0.72–1.88) for BPS. Interpretation Whereas there were significant associations of BPA exposure with general and abdominal obesity, BPF or BPS, at current exposure level, was not significantly associated with obesity in U.S. adults. Continued biomonitoring of these bisphenols in populations and further investigations on their health effects in humans are warranted.

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Section: Discussionmentioning

confidence: 99%

Bisphenol A substitutes and obesity in US adults: analysis of a population-based, cross-sectional study

Liu

Lehmler

Sun

et al. 2017

The Lancet Planetary Health

141

100

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“…That article also ran a series of experiments blocking several estrogen receptors, which then significantly blocked lipid accumulation. The study went on to propose that BPS is causing lipid accumulation and promoting the differentiation of preadipose cells via the peroxisome proliferator-activated receptor-γ (PPARG) pathway [34]. The second article of that year reported exactly the same results with regard to increased lipid accumulation and several increased adipogenic markers, but they used Murine 3T3-L1 preadipocytes.…”

Section: Dietary Bps Exposure and Obesogenic Effects/metabolic Disordersmentioning

confidence: 94%

Bisphenol S in Food Causes Hormonal and Obesogenic Effects Comparable to or Worse than Bisphenol A: A Literature Review

et al. 2020

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In recent years, bisphenol analogues such as bisphenol S (BPS) have come to replace bisphenol A in food packaging and food containers, since bisphenol A (BPA) has been shown to leach into food and water, causing numerous negative health effects. Unfortunately, little or no research was done to determine the safety of these BPA-free products before they were marketed to the public as a healthier alternative. The latest studies have shown that some of these bisphenol analogues may be even more harmful than the original BPA in some situations. This article used a literature survey to investigate the bisphenol analogue BPS and compare it to BPA and other analogues with regards to increased obesity, metabolic disorders, cancer, and reproductive defects; among others. It was found that BPS works via different pathways than does BPA while causing equivalent obesogenic effects, such as activating preadipocytes, and that BPS was correlated with metabolic disorders, such as gestational diabetes, that BPA was not correlated with. BPS was also shown to be more toxic to the reproductive system than BPA and was shown to hormonally promote certain breast cancers at the same rate as BPA. Therefore, a strong argument may be made to regulate BPS in exactly the same manner as BPA.

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“…We and others have previously shown that BPA [ 17 – 20 ] and its metabolite BPA-glucuronide (BPA-G) induce lipid accumulation and adipogenesis in vitro [ 19 ]. Moreover, we have also reported that BPS is adipogenic in human primary preadipocytes, where it induced lipid accumulation and expression of adipogenic genes both at high and at environmentally relevant concentration [ 21 ]. In addition, we and others have shown that BPS treatment increased lipid metabolism, glucose uptake and adipogenesis in the murine 3T3L1 preadipocyte cell line [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A and Bisphenol S Induce Distinct Transcriptional Profiles in Differentiating Human Primary Preadipocytes

et al. 2016

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Bisphenol S (BPS) is increasingly used as a replacement plasticizer for bisphenol A (BPA) but its effects on human health have not been thoroughly examined. Recent evidence indicates that both BPA and BPS induce adipogenesis, although the mechanisms leading to this effect are unclear. In an effort to identify common and distinct mechanisms of action in inducing adipogenesis, transcriptional profiles of differentiating human preadipocytes exposed to BPA or BPS were compared. Human subcutaneous primary preadipocytes were differentiated in the presence of either 25 μM BPA or BPS for 2 and 4 days. Poly-A RNA-sequencing was used to identify differentially expressed genes (DEGs). Functional analysis of DEGs was undertaken in Ingenuity Pathway Analysis. BPA-treatment resulted in 472 and 176 DEGs on days 2 and 4, respectively, affecting pathways such as liver X receptor (LXR)/retinoid X receptor (RXR) activation, hepatic fibrosis and cholestasis. BPS-treatment resulted in 195 and 51 DEGs on days 2 and 4, respectively, revealing enrichment of genes associated with adipogenesis and lipid metabolism including the adipogenesis pathway and cholesterol biosynthesis. Interestingly, the transcription repressor N-CoR was identified as a negative upstream regulator in both BPA- and BPS-treated cells. This study presents the first comparison of BPA- and BPS-induced transcriptional profiles in human differentiating preadipocytes. While we previously showed that BPA and BPS both induce adipogenesis, the results from this study show that BPS affects adipose specific transcriptional changes earlier than BPA, and alters the expression of genes specifically related to adipogenesis and lipid metabolism. The findings provide insight into potential BPS and BPA-mediated mechanisms of action in inducing adipogenesis in human primary preadipocytes.

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Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors

Cited by 116 publications

References 50 publications

Bisphenol A substitutes and obesity in US adults: analysis of a population-based, cross-sectional study

Bisphenol A substitutes and obesity in US adults: analysis of a population-based, cross-sectional study

Bisphenol S in Food Causes Hormonal and Obesogenic Effects Comparable to or Worse than Bisphenol A: A Literature Review

Bisphenol A and Bisphenol S Induce Distinct Transcriptional Profiles in Differentiating Human Primary Preadipocytes

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