蛋鸡脂肪肝出血综合征(FLHS)是蛋鸡体内脂肪代谢紊乱引起的以肝脏发生脂肪病变、出血、产蛋率下降为主要特征的营养代谢疾病，是高产蛋鸡常见多发病。高能、高脂等营养因素仍是蛋鸡生产中诱发蛋鸡脂肪肝出血综合征主要病因，但其发病机制尚不清楚。越来越多研究表明，Insulin/PI3K/Akt信号通路紊乱是人类多种代谢疾病（肥胖、非酒精性脂肪肝、代谢综合征）发病的分子机制。本研究采用高能低蛋白日粮建立蛋鸡脂肪肝出血综合征模型，并通过动物临床实验和体外实验，研究Insulin/PI3K/Akt信号通路与FLHS关系，探讨Insulin/PI3K/Akt信号通路对蛋鸡脂肪肝出血综合征作用机制以及抗脂因子的干扰机制；为蛋鸡脂肪肝出血综合征发病机理的研究提供新的分子生物学依据，并从比较医学上，对人类胰岛素抵抗相关疾病研究提供参考。

Fatty liver hemorrhagic syndrome (FLHS) is a nutritional and metabolic disease characterized by excessive fat in the liver of prolific laying hens, associated with varying degrees of hemorrhage and reduction of egg production. A surfeit of energy, such as excessive fat or carbohydrates in the diets is the main cause of fatty liver hemorrhagic syndrome in laying hens, but its pathogenesis is not well understood. Accumulating evidences indicate that deregulation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway is a common molecular event associated with metabolic dysfunctions including obesity, metabolic syndrome, and the NAFLD. Therefore, this study establishes a model of fatty liver hemorrhagic syndrome by high-energy low-protein diet, and to reveal the relationships between Insulin/PI3K/Akt signaling pathways and FLHS in vitro and in vivo, and to explore the exact regulatory mechanism of Insulin/PI3K/AKT signaling pathway to prevent and control FLHS by lipotropism-factors. The value and novelty of this study is to elucidate the pathogenesis and prevention mechanism of FLHS by novel evidence of insulin and its signaling pathway on the molecular level. Moreover, this study also provides reference for insulin resistant related diseases of humans in Comparative Medicine.