Bisphenol A disturbs hepatic apolipoprotein A1 expression and cholesterol metabolism in rare minnow Gobiocypris rarus

Bisphenol A (BPA) is a well-known plasticizer, which is widely distributed in the aquatic environment. Lots of studies showed that BPA could lead to lipid metabolism disorder in fish, but few studies studied the mechanism from the perspective of lipid transport. Apolipoprotein A1 (ApoA1) is the main component of high-density lipoprotein (HDL), and plays important roles in reverse cholesterol transport (RCT). In this study, we investigated the effect and molecular mechanism of BPA on ApoA1 and its effect on cholesterol in adult male rare minnow. Results showed that BPA could disturb hepatic ApoA1 expression through regulating Esrrg recruitment and DNA methylation in its promoter region, and ultimately up-regulated ApoA1 protein levels. The increased hepatic ApoA1 improved HDL-C levels, enhanced RCT, and disrupted cholesterol levels. The present study reveals the effect and mechanism of BPA on fish cholesterol metabolism from the perspective of cholesterol transport.

Automated summary

The study found that BPA can disrupt hepatic ApoA1 expression by regulating Esrrg recruitment and DNA methylation, ultimately increasing ApoA1 protein levels. This leads to elevated hepatic ApoA1 levels, improved HDL-C levels, enhanced RCT, and disturbed cholesterol levels.