In vitro study on the role of reduced lipid degradation capacity induced by bisphenol F in triggering lipid accumulation in nonalcoholic fatty liver disease

  Objective  From the perspective of lipid degradation, the effects of bisphenol F (BPF) exposure on lipolysis, fatty acid oxidation, and reactive oxygen species (ROS) levels in HepG2 cells were described.

  Methods  HepG2 cells were used to construct an in vitro exposure model. The effects of BPF on the lipid degradation pathway were observed by real-time quantitative PCR, confocal microscopy, and Western blot.

  Results  BPF exposure reduced the mRNA and protein expression of the rate-limiting enzymes, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in HepG2 cells (P < 0.05). The mRNA and protein expressions of the fatty acid oxidation-related proteins, carnitine palmitoyl transferase 1α (CPT1α) and peroxisome proliferator-activated receptor α (PPAR α), were decreased (P < 0.05), and the ROS level from mitochondria was increased (P < 0.01). This caused the accumulation of lipid droplets.

  Conclusions  BPF exposure reduced lipolysis and fatty acid oxidation in HepG2 cells and increased the level of ROS derived from mitochondria, which may be one of the important reasons for the occurrence of nonalcoholic fatty liver disease (NAFLD)-like changes.