Low-Dose Bisphenol-A Impairs Adipogenesis and Generates Dysfunctional 3T3-L1 Adipocytes
Environmental endocrine disruptors (EDCs), including bisphenol-A (BPA), have been recently involved in obesity and diabetes by dysregulating adipose tissue function. Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. The...
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| Veröffentlicht in: | PloS one 2016-03, Vol.11 (3), p.e0150762-e0150762 |
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| creator | Ariemma, Fabiana D'Esposito, Vittoria Liguoro, Domenico Oriente, Francesco Cabaro, Serena Liotti, Antonietta Cimmino, Ilaria Longo, Michele Beguinot, Francesco Formisano, Pietro Valentino, Rossella |
| description | Environmental endocrine disruptors (EDCs), including bisphenol-A (BPA), have been recently involved in obesity and diabetes by dysregulating adipose tissue function. Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. Therefore, 3T3-L1 pre-adipocytes were cultured for three weeks with BPA 1 nM to mimic human environmental exposure. We evaluated BPA effect on cell proliferation, differentiation, gene expression and adipocyte metabolic function. BPA significantly increased pre-adipocyte proliferation (p |
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Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. Therefore, 3T3-L1 pre-adipocytes were cultured for three weeks with BPA 1 nM to mimic human environmental exposure. We evaluated BPA effect on cell proliferation, differentiation, gene expression and adipocyte metabolic function. BPA significantly increased pre-adipocyte proliferation (p<0.01). In 3T3-L1 adipocytes differentiated in the presence of BPA, the expression of Peroxisome proliferator-activated receptor gamma (PPARγ), Fatty Acid Binding Protein 4/Adipocyte Protein 2 (FABP4/AP2) and CCAAT/enhancer binding protein (C/EBPα) was increased by 3.5, 1.5 and 3 folds, respectively. Mature adipocytes also showed a significant increase in lipid accumulation (p<0.05) and alterations of insulin action, with significant reduction in insulin-stimulated glucose utilization (p<0.001). Moreover, in mature adipocytes, mRNA levels of Leptin, interleukin-6 (IL6) and interferon-γ (IFNγ) were significantly increased (p<0.05). In conclusion, BPA prolonged exposure at low doses, consistent with those found in the environment, may affect adipocyte differentiation program, enhancing pre-adipocyte proliferation and anticipating the expression of the master genes involved in lipid/glucose metabolism. The resulting adipocytes are hypertrophic, with impaired insulin signaling, reduced glucose utilization and increased pro-inflammatory cytokine expression. Thus, these data supported the hypothesis that BPA exposure, during critical stages of adipose tissue development, may cause adipocyte metabolic dysfunction and inflammation, thereby increasing the risk of developing obesity-related diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0150762</identifier><identifier>PMID: 26942597</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3T3-L1 Cells ; Adipocytes ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipocytes - pathology ; Adipogenesis ; Adipogenesis - drug effects ; Adipogenesis - genetics ; Adipose tissue ; Animals ; Benzhydryl Compounds - toxicity ; Biology and Life Sciences ; Biomarkers - metabolism ; Bisphenol A ; CCAAT/enhancer-binding protein ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell proliferation ; Cell Proliferation - drug effects ; Councils ; Development and progression ; Diabetes ; Diabetes mellitus ; Differentiation (biology) ; Endocrine disruptors ; Endocrinology ; Eutrophication ; Exposure ; Fatty acid-binding protein ; Fatty acids ; Gene expression ; Gene Expression Regulation - drug effects ; Glucose ; Glucose - metabolism ; Health risks ; Inflammation ; Inflammation - pathology ; Inflammation Mediators - metabolism ; Insulin ; Insulin - metabolism ; Interferon ; Interleukin 6 ; Leptin ; Lipid Droplets - drug effects ; Lipid Droplets - metabolism ; Lipid metabolism ; Lipid Metabolism - drug effects ; Lipids ; Medicine and Health Sciences ; Metabolism ; Mice ; Obesity ; Oncology ; Phenols ; Phenols - toxicity ; Physiological aspects ; Proteins ; Public health ; Real-Time Polymerase Chain Reaction ; Risk factors ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Signaling ; γ-Interferon</subject><ispartof>PloS one, 2016-03, Vol.11 (3), p.e0150762-e0150762</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Ariemma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Ariemma et al 2016 Ariemma et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c585t-75e0a758333d138c366ff99cd5a7d70819841734f5a59c80855012000ee49b453</citedby><cites>FETCH-LOGICAL-c585t-75e0a758333d138c366ff99cd5a7d70819841734f5a59c80855012000ee49b453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778877/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778877/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26942597$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ariemma, Fabiana</creatorcontrib><creatorcontrib>D'Esposito, Vittoria</creatorcontrib><creatorcontrib>Liguoro, Domenico</creatorcontrib><creatorcontrib>Oriente, Francesco</creatorcontrib><creatorcontrib>Cabaro, Serena</creatorcontrib><creatorcontrib>Liotti, Antonietta</creatorcontrib><creatorcontrib>Cimmino, Ilaria</creatorcontrib><creatorcontrib>Longo, Michele</creatorcontrib><creatorcontrib>Beguinot, Francesco</creatorcontrib><creatorcontrib>Formisano, Pietro</creatorcontrib><creatorcontrib>Valentino, Rossella</creatorcontrib><title>Low-Dose Bisphenol-A Impairs Adipogenesis and Generates Dysfunctional 3T3-L1 Adipocytes</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Environmental endocrine disruptors (EDCs), including bisphenol-A (BPA), have been recently involved in obesity and diabetes by dysregulating adipose tissue function. Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. Therefore, 3T3-L1 pre-adipocytes were cultured for three weeks with BPA 1 nM to mimic human environmental exposure. We evaluated BPA effect on cell proliferation, differentiation, gene expression and adipocyte metabolic function. BPA significantly increased pre-adipocyte proliferation (p<0.01). In 3T3-L1 adipocytes differentiated in the presence of BPA, the expression of Peroxisome proliferator-activated receptor gamma (PPARγ), Fatty Acid Binding Protein 4/Adipocyte Protein 2 (FABP4/AP2) and CCAAT/enhancer binding protein (C/EBPα) was increased by 3.5, 1.5 and 3 folds, respectively. Mature adipocytes also showed a significant increase in lipid accumulation (p<0.05) and alterations of insulin action, with significant reduction in insulin-stimulated glucose utilization (p<0.001). Moreover, in mature adipocytes, mRNA levels of Leptin, interleukin-6 (IL6) and interferon-γ (IFNγ) were significantly increased (p<0.05). In conclusion, BPA prolonged exposure at low doses, consistent with those found in the environment, may affect adipocyte differentiation program, enhancing pre-adipocyte proliferation and anticipating the expression of the master genes involved in lipid/glucose metabolism. The resulting adipocytes are hypertrophic, with impaired insulin signaling, reduced glucose utilization and increased pro-inflammatory cytokine expression. Thus, these data supported the hypothesis that BPA exposure, during critical stages of adipose tissue development, may cause adipocyte metabolic dysfunction and inflammation, thereby increasing the risk of developing obesity-related diseases.</description><subject>3T3-L1 Cells</subject><subject>Adipocytes</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipocytes - pathology</subject><subject>Adipogenesis</subject><subject>Adipogenesis - drug effects</subject><subject>Adipogenesis - genetics</subject><subject>Adipose tissue</subject><subject>Animals</subject><subject>Benzhydryl Compounds - toxicity</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers - metabolism</subject><subject>Bisphenol A</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Councils</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Differentiation (biology)</subject><subject>Endocrine disruptors</subject><subject>Endocrinology</subject><subject>Eutrophication</subject><subject>Exposure</subject><subject>Fatty acid-binding protein</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Health risks</subject><subject>Inflammation</subject><subject>Inflammation - pathology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Interferon</subject><subject>Interleukin 6</subject><subject>Leptin</subject><subject>Lipid Droplets - drug effects</subject><subject>Lipid Droplets - metabolism</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ariemma, Fabiana</au><au>D'Esposito, Vittoria</au><au>Liguoro, Domenico</au><au>Oriente, Francesco</au><au>Cabaro, Serena</au><au>Liotti, Antonietta</au><au>Cimmino, Ilaria</au><au>Longo, Michele</au><au>Beguinot, Francesco</au><au>Formisano, Pietro</au><au>Valentino, Rossella</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low-Dose Bisphenol-A Impairs Adipogenesis and Generates Dysfunctional 3T3-L1 Adipocytes</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-03-04</date><risdate>2016</risdate><volume>11</volume><issue>3</issue><spage>e0150762</spage><epage>e0150762</epage><pages>e0150762-e0150762</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Environmental endocrine disruptors (EDCs), including bisphenol-A (BPA), have been recently involved in obesity and diabetes by dysregulating adipose tissue function. Our aim was to examine whether prolonged exposure to low doses of BPA could affect adipogenesis and adipocyte metabolic functions. Therefore, 3T3-L1 pre-adipocytes were cultured for three weeks with BPA 1 nM to mimic human environmental exposure. We evaluated BPA effect on cell proliferation, differentiation, gene expression and adipocyte metabolic function. BPA significantly increased pre-adipocyte proliferation (p<0.01). In 3T3-L1 adipocytes differentiated in the presence of BPA, the expression of Peroxisome proliferator-activated receptor gamma (PPARγ), Fatty Acid Binding Protein 4/Adipocyte Protein 2 (FABP4/AP2) and CCAAT/enhancer binding protein (C/EBPα) was increased by 3.5, 1.5 and 3 folds, respectively. Mature adipocytes also showed a significant increase in lipid accumulation (p<0.05) and alterations of insulin action, with significant reduction in insulin-stimulated glucose utilization (p<0.001). Moreover, in mature adipocytes, mRNA levels of Leptin, interleukin-6 (IL6) and interferon-γ (IFNγ) were significantly increased (p<0.05). In conclusion, BPA prolonged exposure at low doses, consistent with those found in the environment, may affect adipocyte differentiation program, enhancing pre-adipocyte proliferation and anticipating the expression of the master genes involved in lipid/glucose metabolism. The resulting adipocytes are hypertrophic, with impaired insulin signaling, reduced glucose utilization and increased pro-inflammatory cytokine expression. Thus, these data supported the hypothesis that BPA exposure, during critical stages of adipose tissue development, may cause adipocyte metabolic dysfunction and inflammation, thereby increasing the risk of developing obesity-related diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26942597</pmid><doi>10.1371/journal.pone.0150762</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-03, Vol.11 (3), p.e0150762-e0150762 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1770505042 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 3T3-L1 Cells Adipocytes Adipocytes - drug effects Adipocytes - metabolism Adipocytes - pathology Adipogenesis Adipogenesis - drug effects Adipogenesis - genetics Adipose tissue Animals Benzhydryl Compounds - toxicity Biology and Life Sciences Biomarkers - metabolism Bisphenol A CCAAT/enhancer-binding protein Cell Differentiation - drug effects Cell Differentiation - genetics Cell proliferation Cell Proliferation - drug effects Councils Development and progression Diabetes Diabetes mellitus Differentiation (biology) Endocrine disruptors Endocrinology Eutrophication Exposure Fatty acid-binding protein Fatty acids Gene expression Gene Expression Regulation - drug effects Glucose Glucose - metabolism Health risks Inflammation Inflammation - pathology Inflammation Mediators - metabolism Insulin Insulin - metabolism Interferon Interleukin 6 Leptin Lipid Droplets - drug effects Lipid Droplets - metabolism Lipid metabolism Lipid Metabolism - drug effects Lipids Medicine and Health Sciences Metabolism Mice Obesity Oncology Phenols Phenols - toxicity Physiological aspects Proteins Public health Real-Time Polymerase Chain Reaction Risk factors RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction - drug effects Signaling γ-Interferon |
| title | Low-Dose Bisphenol-A Impairs Adipogenesis and Generates Dysfunctional 3T3-L1 Adipocytes |
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