Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors
Human exposure to bisphenol A has been associated with negative health outcomes in humans and its use is now regulated in a number of countries. Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A; however, its effects on cellular metabolism and potential role as an endocrine dis...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2016-04, Vol.157 (4), p.1397-1407 |
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| creator | Boucher, Jonathan G Ahmed, Shaimaa Atlas, Ella |
| description | Human exposure to bisphenol A has been associated with negative health outcomes in humans and its use is now regulated in a number of countries. Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A; however, its effects on cellular metabolism and potential role as an endocrine disruptor have not been fully characterized. In the current study, we evaluated the effect of BPS on adipogenesis in primary human preadipocytes. The effect of BPS on the differentiation of human preadipocytes was determined after treatment with BPS at concentrations ranging from 0.1nM to 25μM by quantifying lipid accumulation and mRNA and protein levels of key adipogenic markers. Treatment of preadipocytes with 25μM BPS induced lipid accumulation and increased the mRNA and protein levels of several adipogenic markers including lipoprotein lipase and adipocyte protein 2 (aP2). Cotreatment of cells with the estrogen receptor antagonist ICI-182,780 significantly inhibited BPS-induced lipid accumulation and affected aP2 but not lipoprotein lipase protein levels. Cotreatment of cells with the glucocorticoid receptor antagonist RU486 had no effect on BPS-induced lipid accumulation or protein levels. Furthermore, reporter gene assays using a synthetic promoter containing peroxisome proliferator-activated receptor-γ (PPARG)-response elements and a PPARG-responsive human aP2 promoter region showed that BPS was able to activate PPARG. To our knowledge, this study is the first to show that BPS induces lipid accumulation and differentiation of primary human preadipocytes, and this effect may be mediated through a PPARG pathway. |
| doi_str_mv | 10.1210/en.2015-1872 |
| format | Article |
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Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A; however, its effects on cellular metabolism and potential role as an endocrine disruptor have not been fully characterized. In the current study, we evaluated the effect of BPS on adipogenesis in primary human preadipocytes. The effect of BPS on the differentiation of human preadipocytes was determined after treatment with BPS at concentrations ranging from 0.1nM to 25μM by quantifying lipid accumulation and mRNA and protein levels of key adipogenic markers. Treatment of preadipocytes with 25μM BPS induced lipid accumulation and increased the mRNA and protein levels of several adipogenic markers including lipoprotein lipase and adipocyte protein 2 (aP2). Cotreatment of cells with the estrogen receptor antagonist ICI-182,780 significantly inhibited BPS-induced lipid accumulation and affected aP2 but not lipoprotein lipase protein levels. Cotreatment of cells with the glucocorticoid receptor antagonist RU486 had no effect on BPS-induced lipid accumulation or protein levels. Furthermore, reporter gene assays using a synthetic promoter containing peroxisome proliferator-activated receptor-γ (PPARG)-response elements and a PPARG-responsive human aP2 promoter region showed that BPS was able to activate PPARG. To our knowledge, this study is the first to show that BPS induces lipid accumulation and differentiation of primary human preadipocytes, and this effect may be mediated through a PPARG pathway.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2015-1872</identifier><identifier>PMID: 27003841</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Accumulation ; Adipocytes - cytology ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipogenesis ; Adipogenesis - drug effects ; Adult ; Bioaccumulation ; Biomarkers ; Bisphenol A ; Blotting, Western ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cells, Cultured ; Differentiation ; Dose-Response Relationship, Drug ; Endocrine disruptors ; Estradiol - analogs & derivatives ; Estradiol - pharmacology ; Estrogen Receptor Antagonists - pharmacology ; Estrogen receptors ; Estrogens ; Fatty Acid-Binding Proteins - genetics ; Fatty Acid-Binding Proteins - metabolism ; Female ; Gene Expression - drug effects ; Glucocorticoid receptors ; Glucocorticoids ; Humans ; Lipase ; Lipid Metabolism - drug effects ; Lipid Metabolism - genetics ; Lipids ; Lipoprotein lipase ; Lipoprotein Lipase - genetics ; Lipoprotein Lipase - metabolism ; Microscopy, Fluorescence ; mRNA ; Peroxisome proliferator-activated receptors ; Phenols - pharmacology ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Preadipocytes ; Protein turnover ; Proteins ; Receptors ; Regulatory sequences ; Reporter gene ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Sulfones - pharmacology</subject><ispartof>Endocrinology (Philadelphia), 2016-04, Vol.157 (4), p.1397-1407</ispartof><rights>Copyright © 2016 by the Endocrine Society</rights><rights>Copyright © 2016 by the Endocrine Society 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-5f4745c4731f078b937752b07577f9ab1fd6f2fabc9a6616243376c8e96e60ab3</citedby><cites>FETCH-LOGICAL-c509t-5f4745c4731f078b937752b07577f9ab1fd6f2fabc9a6616243376c8e96e60ab3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27003841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boucher, Jonathan G</creatorcontrib><creatorcontrib>Ahmed, Shaimaa</creatorcontrib><creatorcontrib>Atlas, Ella</creatorcontrib><title>Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Human exposure to bisphenol A has been associated with negative health outcomes in humans and its use is now regulated in a number of countries. Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A; however, its effects on cellular metabolism and potential role as an endocrine disruptor have not been fully characterized. In the current study, we evaluated the effect of BPS on adipogenesis in primary human preadipocytes. The effect of BPS on the differentiation of human preadipocytes was determined after treatment with BPS at concentrations ranging from 0.1nM to 25μM by quantifying lipid accumulation and mRNA and protein levels of key adipogenic markers. Treatment of preadipocytes with 25μM BPS induced lipid accumulation and increased the mRNA and protein levels of several adipogenic markers including lipoprotein lipase and adipocyte protein 2 (aP2). Cotreatment of cells with the estrogen receptor antagonist ICI-182,780 significantly inhibited BPS-induced lipid accumulation and affected aP2 but not lipoprotein lipase protein levels. Cotreatment of cells with the glucocorticoid receptor antagonist RU486 had no effect on BPS-induced lipid accumulation or protein levels. Furthermore, reporter gene assays using a synthetic promoter containing peroxisome proliferator-activated receptor-γ (PPARG)-response elements and a PPARG-responsive human aP2 promoter region showed that BPS was able to activate PPARG. To our knowledge, this study is the first to show that BPS induces lipid accumulation and differentiation of primary human preadipocytes, and this effect may be mediated through a PPARG pathway.</description><subject>Accumulation</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipogenesis</subject><subject>Adipogenesis - drug effects</subject><subject>Adult</subject><subject>Bioaccumulation</subject><subject>Biomarkers</subject><subject>Bisphenol A</subject><subject>Blotting, Western</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - genetics</subject><subject>Cells, Cultured</subject><subject>Differentiation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endocrine disruptors</subject><subject>Estradiol - analogs & derivatives</subject><subject>Estradiol - pharmacology</subject><subject>Estrogen Receptor Antagonists - pharmacology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Fatty Acid-Binding Proteins - genetics</subject><subject>Fatty Acid-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Gene Expression - drug effects</subject><subject>Glucocorticoid receptors</subject><subject>Glucocorticoids</subject><subject>Humans</subject><subject>Lipase</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipid Metabolism - genetics</subject><subject>Lipids</subject><subject>Lipoprotein lipase</subject><subject>Lipoprotein Lipase - genetics</subject><subject>Lipoprotein Lipase - metabolism</subject><subject>Microscopy, Fluorescence</subject><subject>mRNA</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phenols - pharmacology</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Preadipocytes</subject><subject>Protein turnover</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Regulatory sequences</subject><subject>Reporter gene</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Sulfones - pharmacology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1P3DAQhi1UBMuWG-cqUg_toaH-iic-UsoWJKRWhZ4tx5nQoMQO9ubAvydRtkWqQD2NRnr86B2_hJwweso4o5_Rn3LKipyVwPfIimlZ5MCAviErSpnIgXM4JEcp3U-rlFIckEMOlIpSshX5-aVNw2_0octusitfjw5Tdla3Q7hDj6lNWeuzH7HtbXzMLsfezhvaGXCP24ndxNBnG-xth9nX4ENMb8l-Y7uEx7u5Jr82F7fnl_n1929X52fXuSuo3uZFI0EWToJgDYWy0gKg4BWFAqDRtmJNrRre2MppqxRTXAoBypWoFSpqK7EmHxfvEMPDiGlr-jY57DrrMYzJsFKzUnE-PfwvCgC6pDCFWZP3_6D3YYx-OsQIJqgSupSz8NNCuRhSitiYYfkjw6iZazHozVyLmWuZ8Hc76Vj1WP-F__QwAR8WIIzDa6p8pxILib4OLrYeh4gpPad8McATKGKimQ</recordid><startdate>201604</startdate><enddate>201604</enddate><creator>Boucher, Jonathan G</creator><creator>Ahmed, Shaimaa</creator><creator>Atlas, Ella</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201604</creationdate><title>Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors</title><author>Boucher, Jonathan G ; Ahmed, Shaimaa ; Atlas, Ella</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-5f4745c4731f078b937752b07577f9ab1fd6f2fabc9a6616243376c8e96e60ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Accumulation</topic><topic>Adipocytes - cytology</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - metabolism</topic><topic>Adipogenesis</topic><topic>Adipogenesis - drug effects</topic><topic>Adult</topic><topic>Bioaccumulation</topic><topic>Biomarkers</topic><topic>Bisphenol A</topic><topic>Blotting, Western</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - genetics</topic><topic>Cells, Cultured</topic><topic>Differentiation</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endocrine disruptors</topic><topic>Estradiol - analogs & derivatives</topic><topic>Estradiol - pharmacology</topic><topic>Estrogen Receptor Antagonists - pharmacology</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Fatty Acid-Binding Proteins - genetics</topic><topic>Fatty Acid-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Gene Expression - drug effects</topic><topic>Glucocorticoid receptors</topic><topic>Glucocorticoids</topic><topic>Humans</topic><topic>Lipase</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipid Metabolism - genetics</topic><topic>Lipids</topic><topic>Lipoprotein lipase</topic><topic>Lipoprotein Lipase - genetics</topic><topic>Lipoprotein Lipase - metabolism</topic><topic>Microscopy, Fluorescence</topic><topic>mRNA</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phenols - pharmacology</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Preadipocytes</topic><topic>Protein turnover</topic><topic>Proteins</topic><topic>Receptors</topic><topic>Regulatory sequences</topic><topic>Reporter gene</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Sulfones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boucher, Jonathan G</creatorcontrib><creatorcontrib>Ahmed, Shaimaa</creatorcontrib><creatorcontrib>Atlas, Ella</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boucher, Jonathan G</au><au>Ahmed, Shaimaa</au><au>Atlas, Ella</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2016-04</date><risdate>2016</risdate><volume>157</volume><issue>4</issue><spage>1397</spage><epage>1407</epage><pages>1397-1407</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Human exposure to bisphenol A has been associated with negative health outcomes in humans and its use is now regulated in a number of countries. Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A; however, its effects on cellular metabolism and potential role as an endocrine disruptor have not been fully characterized. In the current study, we evaluated the effect of BPS on adipogenesis in primary human preadipocytes. The effect of BPS on the differentiation of human preadipocytes was determined after treatment with BPS at concentrations ranging from 0.1nM to 25μM by quantifying lipid accumulation and mRNA and protein levels of key adipogenic markers. Treatment of preadipocytes with 25μM BPS induced lipid accumulation and increased the mRNA and protein levels of several adipogenic markers including lipoprotein lipase and adipocyte protein 2 (aP2). Cotreatment of cells with the estrogen receptor antagonist ICI-182,780 significantly inhibited BPS-induced lipid accumulation and affected aP2 but not lipoprotein lipase protein levels. Cotreatment of cells with the glucocorticoid receptor antagonist RU486 had no effect on BPS-induced lipid accumulation or protein levels. Furthermore, reporter gene assays using a synthetic promoter containing peroxisome proliferator-activated receptor-γ (PPARG)-response elements and a PPARG-responsive human aP2 promoter region showed that BPS was able to activate PPARG. To our knowledge, this study is the first to show that BPS induces lipid accumulation and differentiation of primary human preadipocytes, and this effect may be mediated through a PPARG pathway.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>27003841</pmid><doi>10.1210/en.2015-1872</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Accumulation Adipocytes - cytology Adipocytes - drug effects Adipocytes - metabolism Adipogenesis Adipogenesis - drug effects Adult Bioaccumulation Biomarkers Bisphenol A Blotting, Western Cell Differentiation - drug effects Cell Differentiation - genetics Cells, Cultured Differentiation Dose-Response Relationship, Drug Endocrine disruptors Estradiol - analogs & derivatives Estradiol - pharmacology Estrogen Receptor Antagonists - pharmacology Estrogen receptors Estrogens Fatty Acid-Binding Proteins - genetics Fatty Acid-Binding Proteins - metabolism Female Gene Expression - drug effects Glucocorticoid receptors Glucocorticoids Humans Lipase Lipid Metabolism - drug effects Lipid Metabolism - genetics Lipids Lipoprotein lipase Lipoprotein Lipase - genetics Lipoprotein Lipase - metabolism Microscopy, Fluorescence mRNA Peroxisome proliferator-activated receptors Phenols - pharmacology PPAR gamma - genetics PPAR gamma - metabolism Preadipocytes Protein turnover Proteins Receptors Regulatory sequences Reporter gene Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - drug effects Signal Transduction - genetics Sulfones - pharmacology |
| title | Bisphenol S Induces Adipogenesis in Primary Human Preadipocytes From Female Donors |
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