Abstract: A variety of metabolism-related diseases can be induced by bisphenol A(BPA), an exogenous endocrine disruptor. The early-life BPA exposure causes nonalcoholic fatty liver disease(NAFLD) in male mice, but whether this effect has a persistent exposure dependence remains unclear. This study was conducted to investigate the mechanism of peroxisome proliferators-activated receptors(PPARs) in regulating BPA-induced hepatic lipid metabolism disorders in mice. Male C57BL/6 mice were selected as experimental subjects, and the experimental groups were set up as control group(saline) and BPA group(500 $ \mu $g/(kg·d) BPA). Drug exposure was performed in 3-week-old mice by gavage until 8 weeks of age, followed by a 56 d withdrawal period. The results showed hepatic lipid accumulation in BPA-exposed mice, which was partially relieved after a 56 d withdrawal period, but serum test results showed that liver damage still existed. The mRNA and Western blotting(WB) results showed that the $ \beta $ protein expression was significantly elevated in three isoforms of PPARs and its target genes stearoyl-coenzyme A desaturase 1(SCD1) and apolipoprotein D(APOD) were differentially expressed (P<0.05). The results showed that PPAR $ \beta $ was involved in regulating the disorders of lipid metabolism in mice caused by BPA exposure, and the upregulation of PPAR $ \beta $ alleviated the symptoms of hepatic lipid accumulation after cessation of exposure.
Keywords: bisphenol A(BPA); metabolic disorders; hepatic lipid accumulation; peroxisome proliferators-activated receptors(PPARs); fatty acid oxidation
合肥工业大学学报自科版