| Title | Fipronil promotes adipogenesis via AMPKα-mediated pathway in 3T3-L1 adipocytes. |
| Publication Type | Journal Article |
| Year of Publication | 2016 |
| Authors | Sun, Q, Qi, W, Yang, JJ, Yoon, KSup, Clark, JM, Park, Y |
| Journal | Food Chem Toxicol |
| Volume | 92 |
| Pagination | 217-23 |
| Date Published | 2016 Jun |
| ISSN | 1873-6351 |
| Keywords | 3T3-L1 Cells, Acetyl-CoA Carboxylase, Adipocytes, Adipogenesis, Aminoimidazole Carboxamide, AMP-Activated Protein Kinases, Animals, CCAAT-Enhancer-Binding Protein-alpha, Cell Differentiation, Cells, Cultured, Gene Expression Regulation, Immunoblotting, Insecticides, Mice, PPAR gamma, Pyrazoles, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Ribonucleotides, RNA, Messenger, Signal Transduction, Triglycerides |
| Abstract | Emerging evidence suggests that organochlorine, organophosphorus and neonicotinoid insecticide exposure may be linked to the development of obesity and type 2 diabetes. However, there is no knowledge of the potential influence of fipronil, which belongs to the phenylpyrazole chemical family, on obesity. Thus, the goal of this study was to determine the role of fipronil in adipogenesis using 3T3-L1 adipocytes. Fipronil treatment, at 10 μM, increased fat accumulation in 3T3-L1 adipocytes as well as promoted key regulators of adipocyte differentiation (CCAAT/enhancer-binding protein α and peroxisome proliferator-activated receptor gamma-γ), and key regulators of lipogenesis (acetyl-CoA carboxylase and fatty acid synthase). The activation of AMPKα with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) abolished effects of fipronil on increased adipogenesis. These results suggest that fipronil alters adipogenesis and results in increased lipid accumulation through a AMPKα-mediated pathway. |
| DOI | 10.1016/j.fct.2016.04.011 |
| Alternate Journal | Food Chem Toxicol |
| PubMed ID | 27103584 |
Veterinary and Animal Sciences