Perfluorobutanesulfonic acid (PFBS) potentiates adipogenesis of 3T3-L1 adipocytes

Food Chem Toxicol. 2018 Oct;120:340-345. doi: 10.1016/j.fct.2018.07.031. Epub 2018 Jul 18.

Abstract

Perfluorobutanesulfonic acid (PFBS) is used as the replacement of perfluorooctanesulfonic acid (PFOS) since 2000 because of the concern on PFOS' persistence in the environment and the bioaccumulation in animals. Accumulating evidence has shown the correlation between the exposure to perfluorinated compounds and enhanced adipogenesis. There is no report, however, of the effect of PFBS on adipogenesis. Therefore, the present work aimed to investigate the role of PFBS in adipogenesis using 3T3-L1 adipocytes. PFBS treatment for 6 days extensively promoted the differentiation of 3T3-L1 preadipocytes to adipocytes, resulting in significantly increased triglyceride levels. In particular, the treatments of PFBS at the early adipogenic differentiation period (day 0-2) were positively correlated with increased the triglyceride accumulation on day 6. PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis. PFBS significantly activated the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) after 4-h treatment, and PFBS' effect on triglyceride was abolished by U0126, a specific MAPK/ERK kinase (MEK) inhibitor. In conclusion, PFBS increased the adipogenesis of 3T3-L1 adipocytes, in part, via MEK/ERK-dependent pathway.

Keywords: 3T3-L1 preadipocyte; Differentiation; ERK; PFAS; PFBS.

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects*
  • Adipocytes / enzymology
  • Adipogenesis / drug effects*
  • Animals
  • Butadienes / pharmacology
  • Cell Differentiation
  • Dose-Response Relationship, Drug
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism*
  • Nitriles / pharmacology
  • Phosphorylation
  • Protein Kinase Inhibitors / pharmacology
  • Real-Time Polymerase Chain Reaction

Substances

  • Butadienes
  • Nitriles
  • Protein Kinase Inhibitors
  • U 0126
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinases