营养配伍失衡导致的严重肝脂沉积，已成为损害养殖鱼类健康的一个重要因素，因此寻找有效的降肝脂调控元件并设计合理的营养调控策略迫在眉睫。PPARα是哺乳动物最为关键的脂分解代谢核调控元件之一，可被食物脂肪酸或药物配基激活。申请人前期工作已证实，鱼类PPARα可被贝特类药物激活，并上调脂分解代谢和发挥降肝脂效应。然而，尚不清楚饲料脂肪酸对鱼类PPARα激活及降肝脂过程和机制。本项目拟以罗非鱼为对象，建立细胞和活体模型，系统研究脂肪酸、脂肪源对罗非鱼PPARα的激活及其降肝脂机制。项目拟重点探究不同单体脂肪酸和不同配比复合脂肪酸对罗非鱼PPARα的激活、以及激活后的细胞/活体代谢机制，并配合以不同饲料油源对不同代谢状态罗非鱼PPARα激活的降肝脂效应进行验证，最终阐明不同脂肪酸在单体和复合状态下激活罗非鱼PPARα并发挥降肝脂效应的生物学机制，为缓解鱼类肝脂沉积提供营养调控策略。

Excessive liver fat deposition caused by imbalance of nutritional compatibility in farmed fish has become a severe issue to aquaculture. It is urgent to find effective targets for lipid-lowering and develop efficient strategies to improve the adverse effects of fat deposition in fish. Peroxisome proliferation activated receptor α (PPARα), which can be activated by fatty acid or peroxisome proliferators, is a master regulator in lipid catabolism of mammals. In fish, it has been reported that PPARα is able to be activated by fibrate drugs and could enhance the lipid catabolism. However, the hypolipidemic effects of PPARα activated by fatty acids have not been fully understood in fish. Therefore, this project is proposed to investigate the lipid-lowering effects of different monomer fatty acids or mixed fatty acids in tilapia PPARα activation in both in vitro and in vivo. As the aim of this project, we hope to uncover the metabolic model of PPARα activated by monomer fatty acids or complex fatty acids with different ratios. Furthermore, we will conduct a feeding experiment to verify and illuminate the biological mechanism of the activation and lipid-lowering model of PPARα by actual oil source of reasonable blended (single oil source/blended oil sources) in tilapia of different metabolic status. The results would provide potential manipulation solutions and basic data for tilapia to relieve liver fat deposition.