脂肪肝病的频繁发生极大制约了罗非鱼养殖业的绿色健康发展。miRNA在肝脏脂代谢调控中发挥了重要作用。项目组前期研究发现，吉富罗非鱼肝脏miR-145-5p在高脂应激下出现异常高表达。生物信息学预测其可能靶向脂代谢关键基因:超长链脂肪酸延伸酶6（ELOVL6）基因。基于此，我们提出如下假说：高脂应激下，吉富罗非鱼肝脏miR-145-5p表达激活，其通过介导ELOVL6基因的表达参与肝脏长链脂肪酸合成代谢，进而造成脂质代谢异常。为验证该假说，本项目拟研究：①验证miR-145-5p靶基因并阐明miR-145-5p对靶基因ELOVL6表达的调控作用；②明确ELOVL6基因在长链脂肪酸合成代谢中的作用机制；③揭示高脂应激下miR-145-5p介导ELOVL6调控脂质代谢的分子响应机制。通过本研究能够深入了解罗非鱼脂代谢的调控机制，为今后缓解或预防罗非鱼养殖过程中脂肪肝的发生提供理论基础。

The development of tilapia aquaculture is greatly limited by the frequent occurrence of fatty liver disease. miRNAs play an important role in regulating hepatic lipid metabolism. Our preliminary study found that high-fat stress caused abnormally high expression of miR-145-5p in the liver of genetically improved farmed tilapia (GIFT, Oreochromis niloticus). Bioinformatics analysis predicted that it may target a key gene of lipid metabolism: elongase of very long chain fatty acid 6 (ELOVL6). Based on these ideas, we propose the following hypothesis: The expression of miR-145-5p in the liver of GIFT is activated under high-fat stress. It participates in the synthesis of long-chain fatty acids in the liver through mediating the expression of the ELOVL6 and thereby causing abnormal lipid metabolism. To verify this hypothesis, this project intends to study: ①Verify relationship between miR-145-5p and its target gene ELOVL6; ②Clarify the function mechanism of ELOVL6 gene in long-chain fatty acid metabolism; ③ Reveal the molecular mechanism of miR-145-5p-ELOVL6 in regulating lipid metabolism under high-fat stress. Our study provides a better understanding of the regulation mechanism involved in GIFT lipid metabolism, and this work may provide a theoretical basis for reducing the occurrence of fatty liver in tilapia farming.