Long-term bisphenol S exposure induces fat accumulation in liver of adult male zebrafish (Danio rerio) and slows yolk lipid consumption in F1 offspring.

Bisphenol S (BPS), as a substitute for bisphenol A, was frequently detected in human urine and blood. It has been reported that BPS could disrupt fat metabolism in vivo and vitro although mechanisms remain unclear. Additionally, there is no study that the disruptive effect of BPS on parental fat metabolism indirectly interferes with the lipid metabolism of offspring. Here, after 120-d exposure to 1, 10, 100, and 1000 μg/L BPS, the transcription level of genes involved in lipid metabolism in liver and feeding regulation of brain-gut axis, as well as the hepatic triacylglycerol (TAG) and plasma lipid levels were investigated in both male and female zebrafish. Results showed that in male liver, fatty acid synthesis and degradation were inhibited by reducing transcription levels of srebp1 and pparα, and the synthesis of TAG was significantly increased using fatty acid as a precursor by elevating agpat4 and dgat2 mRNA expression levels. As a consequence, fat accumulation and the increased TAG levels were observed in male liver, and lipid levels were also elevated in male plasma. In female liver, there was no excessive fat accumulation and BPS exposure had a non-monotonic effect on the gene expression of fasn, dagt2, and pparα. Notably, the unexposed offspring showed a large amount of yolk lipid remain at 5 days post fertilization. This study obviously demonstrated that long-term BPS exposure increases the risk of non-alcoholic fatty liver disease in male zebrafish and life-cycle exposure hazard on offspring is noteworthy.

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