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10.1289/ehp.1409143 http://scihub22266oqcxt.onion/10.1289/ehp.1409143 C4671229!4671229 !26018136     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26018136 &cmd=llinks): Failed to open stream: HTTP request failed! 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In Vitro Effects of Bisphenol A ?-D-Glucuronide (BPA-G) on Adipogenesis in Human and Murine Preadipocytes |pdf=|usr=}}{{26018136 }} gab.com Text In Vitro Effects of Bisphenol A -D-Glucuronide (BPA-G) on Adipogenesis in Human and Murine Preadipocytes JO: Environ Health Perspect http://www.kidney.de/pget.php?&tw=1&pmid=26018136 #FOAvip BACKGROUND: Exposure to common environmental substances, such as bisphenol A (BPA), has been associated with a number of negative health outcomes. In vivo, BPA is rapidly converted to its predominant metabolite, BPA-glucuronide (BPA-G), which has long been believed to be biologically inactive because it lacks estrogenic activity. However, the effects of BPA-G on cellular metabolism have not been characterized. In the present study we examined the effect of BPA-G on adipogenesis. METHODS: The effect of BPA-G on the differentiation of human and 3T3L1 murine preadipocytes was evaluated in vitro by quantifying lipid accumulation and the expression of adipogenic markers. RESULTS: Treatment of 3T3L1 preadipocytes with 10 ?M BPA-G induced a significant increase in lipid accumulation, mRNA expression of the adipogenic markers sterol regulatory element binding factor 1 (SREBF1) and lipoprotein lipase (LPL), and protein levels of LPL, aP2, and adipsin. Treatment of primary human preadipocytes with BPA-G also induced adipogenesis as determined by aP2 levels. Co-treatment of cells with the estrogen receptor (ER) antagonist fulvestrant (ICI) significantly inhibited the BPA-G-induced increase in LPL and aP2 levels, whereas treatment with ICI alone had no effect. Moreover, BPA-G did not display any significant estrogenic activity. CONCLUSIONS: To our knowledge, this study is the first to report that BPA-G induces adipocyte differentiation and is not simply an inactive metabolite. The fact that BPA-G induced adipogenesis and was inhibited by an ER antagonist yet showed no estrogenic activity suggests that it has no classical ER transcriptional activation function and acts through a pathway that remains to be determined. Twit Text FOAVip In Vitro Effects of Bisphenol A -D-Glucuronide (BPA-G) on Adipogenesis in Human and Murine Preadipocytes ????Environ Health Perspect http://www.kidney.de/pget.php?&tw=1&pmid=26018136 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26018136 #FOAvip English Wikipedia <ref>{{Cite pmid|26018136 }}</ref> In Vitro Effects of Bisphenol A ?-D-Glucuronide (BPA-G) on Adipogenesis in Human and Murine Preadipocytes #MMPMID26018136 Boucher JG ; Boudreau A ; Ahmed S ; Atlas E Environ Health Perspect 2015[Dec]; 123 (12 ): 1287-93 PMID26018136 show ga BACKGROUND: Exposure to common environmental substances, such as bisphenol A (BPA), has been associated with a number of negative health outcomes. In vivo, BPA is rapidly converted to its predominant metabolite, BPA-glucuronide (BPA-G), which has long been believed to be biologically inactive because it lacks estrogenic activity. However, the effects of BPA-G on cellular metabolism have not been characterized. In the present study we examined the effect of BPA-G on adipogenesis. METHODS: The effect of BPA-G on the differentiation of human and 3T3L1 murine preadipocytes was evaluated in vitro by quantifying lipid accumulation and the expression of adipogenic markers. RESULTS: Treatment of 3T3L1 preadipocytes with 10 ?M BPA-G induced a significant increase in lipid accumulation, mRNA expression of the adipogenic markers sterol regulatory element binding factor 1 (SREBF1) and lipoprotein lipase (LPL), and protein levels of LPL, aP2, and adipsin. Treatment of primary human preadipocytes with BPA-G also induced adipogenesis as determined by aP2 levels. Co-treatment of cells with the estrogen receptor (ER) antagonist fulvestrant (ICI) significantly inhibited the BPA-G-induced increase in LPL and aP2 levels, whereas treatment with ICI alone had no effect. Moreover, BPA-G did not display any significant estrogenic activity. CONCLUSIONS: To our knowledge, this study is the first to report that BPA-G induces adipocyte differentiation and is not simply an inactive metabolite. The fact that BPA-G induced adipogenesis and was inhibited by an ER antagonist yet showed no estrogenic activity suggests that it has no classical ER transcriptional activation function and acts through a pathway that remains to be determined. |3T3-L1 Cells [MESH] |Adipocytes/cytology/*drug effects/metabolism [MESH] |Adipogenesis/drug effects [MESH] |Animals [MESH] |Benzhydryl Compounds/*pharmacology [MESH] |Cell Differentiation/drug effects [MESH] |Cells, Cultured [MESH] |Estradiol/analogs & derivatives/pharmacology [MESH] |Estrogen Receptor Antagonists/pharmacology [MESH] |Fulvestrant [MESH] |Gene Expression Regulation [MESH] |Glucuronides/*pharmacology [MESH] |Humans [MESH] |Lipid Metabolism [MESH] |Mice [MESH] |Phenols/*pharmacology [MESH]In Vitro Effects of Bisphenol A ?-D-Glucuronide (BPA-G) on Adipogenesi(epmc).pdf DeepDyve Pubget Overpricing