Endocrine Disruptor Bisphenol A Induces Expression of Peroxisome Proliferator-Activated Receptor γ which Contributes to Down-Regulation of FSH-Stimulated Aromatase Expression and Estradiol Production in Human Granulosa KGN Cells.

2008 ◽  
Vol 78 (Suppl_1) ◽  
pp. 199-199
Author(s):  
Jakub Kwintkiewicz ◽  
Linda C. Giudice
Keyword(s):  
Bisphenol A ◽  
Endocrine Disruptor ◽  
Peroxisome Proliferator ◽  
Down Regulation ◽  
Aromatase Expression ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Myricetin Increases Hepatic Peroxisome Proliferator-Activated ReceptorαProtein Expression and Decreases Plasma Lipids and Adiposity in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Chia Ju Chang ◽  
Thing-Fong Tzeng ◽  
Shorong-Shii Liou ◽  
Yuan-Shiun Chang ◽  
I-Min Liu
Keyword(s):  
Plasma Lipids ◽  
Regulatory Element ◽  
Plasma Lipid ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Down Regulation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Once Daily ◽  
Sterol Regulatory Element ◽  
Lowered Body

The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of myricetin. Myricetin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3T3-L1 adipocytes. The high-fat diet (HFD)-fed rats were dosed orally with myricetin or fenofibrate, once daily for eight weeks. Myricetin (300 mg kg−1per day) displayed similar characteristics to fenofibrate (100 mg kg−1per day) in reducing lowered body weight (BW) gain, visceral fat-pad weights and plasma lipid levels of HFD-fed rats. Myricetin also reduced the hepatic triglyceride and cholesterol contents, as well as lowered hepatic lipid droplets accumulation and epididymal adipocyte size in HFD-fed rats. Myricetin and fenofibrate reversed the HFD-induced down-regulation of the hepatic peroxisome proliferator activated receptor (PPAR)α. HFD-induced decreases of the hepatic protein level of acyl-CoA oxidase and cytochrome P450 isoform 4A1 were up-regulated by myricetin and fenofibrate. The elevated expressions of hepatic sterol regulatory element binding proteins (SREBPs) of HFD-fed rats were lowered by myricetin and fenofibrate. These results suggest that myricetin suppressed BW gain and body fat accumulation by increasing the fatty acid oxidation, which was likely mediated via up-regulation of PPARαand down-regulation of SREBP expressions in the liver of HFD-fed rats.

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.

scholarly journals Egr-1 contributes to IL-1-mediated down-regulation of peroxisome proliferator-activated receptor γ expression in human osteoarthritic chondrocytes

2012 ◽  
Vol 14 (2) ◽  
pp. R69 ◽  
Author(s):  
Sarah-Salwa Nebbaki ◽  
Fatima El Mansouri ◽  
Hassan Afif ◽  
Mohit Kapoor ◽  
Mohamed Benderdour ◽  
...  
Keyword(s):  
Peroxisome Proliferator ◽  
Down Regulation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Osteoarthritic Chondrocytes
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