丁酸在亚急性瘤胃酸中毒和动物健康方面作用机制的研究进展

Research Progress on Mechanism of Butyrate in Subacute RuminalAcidosis and Animal Health

反刍动物饲喂高谷物饲粮易诱发亚急性瘤胃酸中毒(SARA),导致采食量和消化率降低,瘤胃和肠上皮的黏膜屏障受损,肝脏脓肿和炎症反应增加。丁酸作为微生物的发酵产物和上皮细胞的能量来源,影响瘤胃液pH和胃肠道微生物区系,促进上皮生长发育。作为信号分子,丁酸参与多个信号通路,在细胞功能、信号转导、机体免疫等方面发挥作用。丁酸通过激活G蛋白偶联受体(GPR)引起多种转录因子的活化,或者作为组蛋白去乙酰化酶(HDAC)抑制剂在基因表达的表观遗传调控中发挥作用。本文综述了丁酸尤其是在高谷物饲粮中添加丁酸盐对反刍动物瘤胃、肠道和肝脏的影响以及分子作用机制,为缓解SARA的危害提供理论依据。

Feeding high-grain diets in ruminants can easily induce subacute ruminal acidosis(SARA),leading to reduced feed intake and digestibility,damage to the mucosal barrier of ruminal and intestinal epithelium,liver abscess and inflammation increase.As a fermentation product of microorganisms and an energy source for epithelium,butyrate affects ruminal pH and gastrointestinal microflora,and promotes epithelial growth and development.As a signal molecule,butyrate participates in multiple signal pathways and plays a role in cell function,signal transduction and body immunity and so on.Butyrate activates many transcription factors by activating G protein coupled receptors(GPR),or acts as a histone deacetylase(HDAC)inhibitor in epigenetic regulation of gene expression.This paper reviews the effects of butyrate,especially added in high-grain diets,on ruminant rumen,intestines and liver,as well as the molecular mechanism of action,to provide a theoretical basis for alleviating the harm of SARA.