期刊
TOXICOLOGY LETTERS
卷 238, 期 2, 页码 65-71出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2015.07.009
关键词
3T3-L1; Adipogenesis; p,p '-DDE; Organochlorine insecticides
类别
资金
- Center for Environmental Health Sciences
- National Institute of Environmental Health Sciences (NIEHS) of the National Institutes of Health (NIH) [R15ES019742]
The incidence of obesity is increasing worldwide at an alarming rate. Recently, exposure to environmental contaminants, especially organochlorines such as p,p'-dichlorodiphenyldichloroethylene (DDE), has been implicated as a possible causative factor in the increasing obesity epidemic. The objective of this study was to evaluate the ability of DDE to alter adipogenesis in a model of sub-optimal differentiation. 3T3-L1 preadipocytes were induced to differentiate in the presence of DDE (0.01-100 mu M) using a sub-optimal differentiation cocktail. Eight days after the initiation of differentiation, adipogenesis was assessed through neutral lipid staining, triglyceride accumulation, and expression of markers of terminal differentiation. Exposure to DDE induced a concentration dependent increase in intracellular neutral lipid accumulation as determined by Oil Red O staining and triglyceride assay. Alterations in lipid accumulation were accompanied by upregulation of genetic markers of differentiation. DDE (10 mu M) enhanced expression of fatty acid binding protein 4 and Sterol regulatory element-binding protein-1c at the 2.5 and 20 mu M concentrations. DDE (2.5, 10, and 20 mu M) induced upregulation of leptin and fatty acid synthase, as compared to sub-optimal vehicle control (0.05% ethanol). Our results indicate that DDE is capable of enhancing adipogenesis and intracellular lipid accumulation in 3T3-L1 cells through upregulation of molecular targets responsible for lipid storage. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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