scholarly journals Bisphenol S- and bisphenol A-induced adipogenesis of murine preadipocytes occurs through direct peroxisome proliferator-activated receptor gamma activation

2016 ◽  
Vol 40 (10) ◽  
pp. 1566-1573 ◽  
Author(s):  
S Ahmed ◽  
E Atlas
Keyword(s):  
Bisphenol A ◽  
Peroxisome Proliferator ◽  
Gamma Activation ◽  
Bisphenol S ◽  
Peroxisome Proliferator Activated Receptor ◽  
Murine Preadipocytes

scholarly journals Bisphenol A enhances adipogenic differentiation of human adipose stromal/stem cells

2014 ◽  
Vol 53 (3) ◽  
pp. 345-353 ◽  
Author(s):  
Jason F Ohlstein ◽  
Amy L Strong ◽  
John A McLachlan ◽  
Jeffrey M Gimble ◽  
Matthew E Burow ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bisphenol A ◽  
Leucine Zipper ◽  
Adipogenic Differentiation ◽  
Density Measurement ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Enhancer Binding Protein ◽  
Pm 10 ◽  
Stromal Stem Cells

Exposure of humans to the endocrine disrupter bisphenol A (BPA) has been associated with increased weight and obesity. However, the mechanism(s) by which BPA increases adipose tissue in humans remains to be determined. The goal of this study was to determine the effects of BPA on adipogenesis of cultured human adipose stromal/stem cells (ASCs), precursors to mature adipocytes. ASCs from three donors were cultured for either 14 or 21 days in adipogenic differentiation media containing increasing concentrations of BPA (100 pM–10 μM). The extent of adipogenic differentiation in the ASCs was assessed by staining with Oil Red O to visualize adipogenic differentiation and then quantified by extraction and optical density measurement of the retained dye. BPA significantly enhanced adipogenesis at a concentration of 1 μM after 21 days of culture. Additionally, we found that BPA increased transcription of the estrogen receptor (ER (ESR1)) and that treatment with the ER antagonist ICI 182 780, blocked the effects of BPA, indicating that BPA may act via an ER-mediated pathway. The results of molecular analyses indicated that the expression of the adipogenesis-associated genes dual leucine zipper-bearing kinase (DLK (MAP3K12)), IGF1, CCAAT/enhancer-binding protein alpha (C/EBPα (CEBPA)), peroxisome proliferator-activated receptor gamma (PPARγ (PPARG)), and lipoprotein lipase (LPL) was temporally accelerated and increased by BPA. In summary, these results indicate that BPA significantly enhances adipogenesis in ASCs through an ER-mediated pathway at physiologically relevant concentrations.

scholarly journals Low-dose Bisphenol-A Promotes Epigenetic Changes at Pparγ Promoter in Adipose Precursor Cells

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3498
Author(s):  
Michele Longo ◽  
Federica Zatterale ◽  
Jamal Naderi ◽  
Cecilia Nigro ◽  
Francesco Oriente ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Promoter Methylation ◽  
Low Dose ◽  
Precursor Cells ◽  
Peroxisome Proliferator ◽  
Epigenetic Changes ◽  
Obesity Prevalence ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pparγ Expression

Exposure to endocrine-disrupting chemicals such as Bisphenol-A (BPA) is associated with an increase in obesity prevalence. Diet is the primary cause of human exposure to this contaminant. BPA promotes obesity by inducing adipocyte dysfunction and altering adipogenesis. Contradictory evidence and unanswered questions are reported in the literature concerning the BPA effects on adipogenesis. To clarify this issue, we tested the effects of prolonged low-dose BPA exposure on different phases of adipogenesis in committed 3T3L1 and uncommitted NIH3T3 preadipocytes. Our findings show that BPA effects on the adipogenesis are mediated by epigenetic mechanisms by reducing peroxisome proliferator-activated receptor gamma (Pparγ) promoter methylation in preadipocytes. Nevertheless, in BPA-exposed 3T3L1, Pparγ expression only transiently increases as lipid accumulation at day 4 of differentiation, without altering the adipogenic potential of the precursor cells. In the absence of differentiation mix, BPA does not make the 3T3L1 an in vitro model of spontaneous adipogenesis and the effects on the Pparγ expression are still limited at day 4 of differentiation. Furthermore, BPA exposure does not commit the NIH3T3 to the adipocyte lineage, although Pparγ overexpression is more evident both in preadipocytes and during the adipocyte differentiation. Interestingly, termination of the BPA exposure restores the Pparγ promoter methylation and inflammatory profile of the 3T3L1 cells. This study shows that BPA induces epigenetic changes in a key adipogenic gene. These modifications are reversible and do not affect preadipocyte commitment and/or differentiation. We identify an alternative transcriptional mechanism by which BPA affects gene expression and demonstrate how the challenge of preventing exposure is fundamental for human health.

Depot-Specific Analysis of Human Adipose Cells and Their Responses to Bisphenol S

Endocrinology ◽  
2020 ◽  
Vol 161 (6) ◽  
Author(s):  
Vian Peshdary ◽  
George Styles ◽  
Rémi Gagné ◽  
Carole L Yauk ◽  
Alexander Sorisky ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Endocrine Disrupting Chemicals ◽  
Environmental Pollutants ◽  
Visceral Obesity ◽  
Gene Expression Profiles ◽  
Peroxisome Proliferator ◽  
Bisphenol S ◽  
Peroxisome Proliferator Activated Receptor ◽  
Adverse Health Outcomes ◽  
Obesity And Diabetes

Abstract Exposure to endocrine-disrupting chemicals (EDCs) is associated with adverse health outcomes including obesity and diabetes. Obesity, and more specifically visceral obesity, is correlated with metabolic disease. The adipose tissue is an endocrine organ and a potential target for many environmental pollutants including bisphenols. The subcutaneous (Sc) and the omental (Om, visceral) depots are composed of mature adipocytes and residing progenitors, which may be different between the depots and may be EDCs targets. Bisphenol A (BPA) is a suspected metabolic disruptor, and is being replaced with structurally similar compounds such as bisphenol S (BPS). Like BPA, BPS induces adipogenesis in murine and primary human Sc preadipocytes. However, the effect of BPS on Om preadipocytes is not known. In this study, we show that human primary progenitors from Om depots have a distinct transcriptomic signature as compared to progenitors derived from donor-matched Sc depots. Furthermore, we show that BPS increases adipogenesis both of Om and Sc preadipocytes and can mimic the action of glucocorticoids or peroxisome proliferator-activated receptor γ (PPARγ) agonists. We also show that BPS treatment, at 0.1 µM and 25 µM, modifies the adipokine profiles both of Om- and Sc-derived adipocytes in a depot-specific manner. Taken together our data show distinct gene expression profiles in the Om vs Sc progenitors and similar responses to the BPA analogue, BPS.

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