Environmental exposure to benzyl butyl phthalate promotes adipogenesis in the preadipocyte 3T3-L1
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2015/03/01
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Description:Obesity is a growing health problem around the world. Convincing evidences suggest that environmental chemicals contribute to the development of obesity, called "Obesogens". Benzyl butyl phthalate (BBP) is used widely in the manufacture of plastics, and has been linked to the development and reproductive toxicity. In this study, we investigated whether BBP exposure promotes adipogenesis in the preadipocyte 3T3-L1 model, and examined the underlying mechanisms. Preadipocyte 3T3-L1 was treated with BBP at doses of 0.1approximately 200.0 microM along with positive controls. Cell viability was measured by Neutral Red uptake assay. The lipid accumulation in 3T3-L1 cells was stained with oil-red, and quantified by AdipoRed fluorescence. Total RNA was extracted during various stages of differentiation, and gene expressions of the adipogenesis associated genes and epigenetic regulated genes were examined by Realtime qPCR. Protein expressions of Acetyl-CoA Carbooxykase (ACC), Adiponectin, C/EBP, Fatty acid synthase (FASN), PARPgamma, and Perilipin were also conducted. BBP showed no significant effect on the cell viability at concentrations of 0.1-100.0 microM after 24 and 48h exposures. BBP significantly induced lipid accumulation dose-dependently. Gene expression of adipogenic transcription factors, PPARgamma, C/EBP, AdipoQ, Adipokines, Fatty acid-binding protein 4 (FABP4) and enzymes that regulate adipogensis, Lipoprotein lipase (LPL), FASN were dose-dependently increased in cells treated with BBP. The protein expression of ACC, adiponectin, C/EBP, LPL, PARPgamma, and Perilipin also showed significant increases as compared with the controls. Furthermore, the multiple genes that modifying chromatin remodeling were also evaluated. Methyl-CpG-binding domain protein was significantly increased in the BBP treated cell during the induction period of differentiation. In summary, BBP is demonstrated to promote adipogenesis dose-dependently through the activation of adipogensis pathway and the modification of epigenetic regulation. [Description provided by NIOSH]
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ISSN:1096-6080
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Pages in Document:365-366
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Volume:144
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Issue:1
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NIOSHTIC Number:nn:20046044
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Citation:Toxicologist 2015 Mar; 144(1):365-366
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Federal Fiscal Year:2015
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Performing Organization:University of Georgia, Athens
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Peer Reviewed:False
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Start Date:20130901
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Source Full Name:The Toxicologist. Society of Toxicology 54th Annual Meeting and ToxExpo, March 22-26, 2015, San Diego, California
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End Date:20160831
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Main Document Checksum:urn:sha-512:54ed3db7d8d748f7bf9ad5c5e14e9de3d5ad2fabe494be691442d3eec4aa2d7267ac85e129c38212357edf48ddb95fd6e14037ff6598d2322a87b1389eaf3a66
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