肠道菌群介导BA-TGR5-cAMP抗炎信号通路调控肉牛脂质重分配的分子机制及锌源调控

肠道菌群介导胆汁酸（BA）-G蛋白胆汁酸偶联受体5（TGR5）-第二信使环磷酸腺苷（cAMP）抗炎信号通路调节机体炎症。BA-TGR5-cAMP途径调控脂质重分配。而机体炎症与脂肪代谢密切相关。但鲜有报道加载不同锌源肠道菌群通过BA-TGR5-cAMP抗炎信号通路调控肉牛脂质重分配的分子机制。本项目拟以肉牛为研究对象，通过日粮添加不同锌源，利用宏基因组学、宏转录组、RT-PCR等研究手段，获取肠道菌群调控BA代谢及BA-TGR5-cAMP抗炎信号通路调控脂质重分配的基础数据，进而利用生物信息学、机器学习算法等分析方法，构建肠道菌群通过BA-TGR5-cAMP抗炎信号通路调控脂质重分配的复杂关系网络及预测模型。旨在利用数学模型解析肠道菌群通过BA-TGR5-cAMP抗炎信号通路调控脂质重分配的分子机制，并从日粮中添加不同锌源的角度调控肉牛肠道健康、肉品质和生产效率提供科学依据。

Intestinal microbiota regulates the inflammatory response of host by bile acid (BA)- takeda G-protein-coupled receptor 5 (TGR5)-second messenger cyclic adenosine monophosphate (cAMP) anti-inflammatory signaling pathway. BA-TGR5-cAMP signaling pathway regulates lipid redistribution. The inflammation response is closely related to lipid metabolism. However, few studies have reported on the molecular mechanism of intestinal microbiota regulating lipid redistribution through BA-TGR5-cAMP anti-inflammatory signaling pathway by supplementation of diverse zinc sources (ZnSdiv) in beef cattle. In present project, set cattle as experimental animals by supplying with ZnSdiv in the diet. The experimental data of intestinal microbiota - mediated BA metabolism pool and lipid redistribution regulated by BA-TGR5-cAMP anti-inflammatory signaling pathway are collected by meta-genomics, meta-transcriptomics, RT-PCR and other research methods. Then, the complex relationship complex network and prediction model of intestinal microbiota regulating lipid redistribution through BA-TGR5-cAMP anti-inflammatory signal pathway were constructed by bioinformatics, machine learning algorithm and other analysis methods. The object of present project is to analyze the molecular regulation mechanism of intestinal microbiota on lipid redistribution by BA-TGR5-cAMP anti-inflammatory signaling pathway, and to provide scientific basis for the nutritional regulation on intestinal health, meat quality and production efficiency of beef cattle from the perspective of dietary ZnSdiv.