Fipronil promotes adipogenesis via AMPKα-mediated pathway in 3T3-L1 adipocytes.

TitleFipronil promotes adipogenesis via AMPKα-mediated pathway in 3T3-L1 adipocytes.
Publication TypeJournal Article
Year of Publication2016
AuthorsSun, Q, Qi, W, Yang, JJ, Yoon, KSup, Clark, JM, Park, Y
JournalFood Chem Toxicol
Date Published2016 Jun
Keywords3T3-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

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.

Alternate JournalFood Chem Toxicol
PubMed ID27103584