Estradiol is a steroid hormone that regulates multiple physiological processes in teleosts. The present study aimed to investigate the role of 17β-estradiol (E2) in lipid metabolism in the liver of Nile tilapia. Waterborne exposures were performed using different concentrations of E2 (0 ng/L, 10 ng/L, 25 ng/L and 50 ng/L) and its receptor inhibitor ICI 182,780 (ICI) (1 μM/L). Subsequently, the survival rate and hepatosomatic index (HSI) of tilapia were measured and no significant changes could be found following E2 exposure. Gene expression of VLDL assembly, lipoprotein lipase and lipoprotein receptor, fatty acid uptake and triacylglycerol metabolism were detected by qPCR. E2 exposure up-regulated the expression of lipid metabolism-related genes MTP, LPL, CD36 and DGAT2. ICI exposure inhibited the level of LDLR in the liver of tilapia. This showed that E2 stimulated the MTP expression and promoted VLDL synthesis. In addition, E2 waterborne exposure induced secretion of LDLR and LPL and promoted fatty acid production. Moreover, E2 up-regulated the expression of CD36 to accelerate the transport of fatty acids. Overall, our study provides new information for evaluating Environmental estrogens (EEs) effects on farming fishes and endocrinological regulation on lipid metabolism in fish.

雌二醇是类固醇激素，可调节硬骨鱼的多个生理过程。本研究旨在调查17β-雌二醇（E2）在尼罗罗非鱼肝脏脂质代谢中的作用。使用不同浓度的E2（0 ng / L，10 ng / L，25 ng / L和50 ng / L）及其受体抑制剂ICI 182,780（ICI）（1μM/ L）进行水接触。随后，测量了罗非鱼的存活率和肝体指数（HSI），暴露于E2后未发现明显变化。通过qPCR检测VLDL组装体的基因表达，脂蛋​​白脂肪酶和脂蛋白受体，脂肪酸摄取和三酰基甘油代谢。E2暴露上调脂质代谢相关基因MTP，LPL，CD36和DGAT2的表达。ICI暴露抑制了罗非鱼肝脏中LDLR的水平。这表明E2刺激MTP表达并促进VLDL合成。另外，E2的水源暴露诱导LDLR和LPL的分泌并促进脂肪酸的产生。此外，E2上调CD36的表达以加速脂肪酸的运输。总的来说，我们的研究为评估环境雌激素对养殖鱼类的影响以及鱼类内脂代谢的内分泌调节提供了新的信息。