FMO3调控犊牛原代肝细胞VLDL-TG的代谢

FMO3 Regulate Very Low Density Lipoprotein-triglyceride Metabolism in Calf Primary Hepatocytes

脂肪肝是围产期奶牛常见的营养代谢性疾病,过多的甘油三酯(TG)无法被极低密度脂蛋白(VLDL)运出肝脏外而导致。含黄素单加氧酶3(FMO3)是近年来发现的与脂代谢相关的重要调控因子。试验通过合成FMO3低表达和过表达腺病毒载体,感染犊牛原代肝细胞,检测FMO3对VLDL组装和分泌过程中关键基因的影响。结果发现,FMO3低表达时VLDL组装与分泌的关键基因mRNA表达量以及VLDL和TG的浓度明显降低,FMO3过表达时结果则相反。研究表明,FMO3能调控犊牛原代肝细胞的VLDL组装和分泌,从而调节细胞内TG的沉积。

Fatty liver was a common nutritional and metabolic disease in perinatal dairy cows. The main cause was that too much TG(triglyceride) cann’t be transported out of the liver by VLDL(very low density lipoprotein).FMO3(flavin containing monooxygenase3) was found as an important regulatory factor related to lipid metabolism in recent years. In this study, adenovirus vectors with low expression and overexpression of FMO3 were synthesized and the effects of FMO3 on key genes in the assembly and secretion of VLDL were detected by infecting calf primary hepatocytes. The results showed that the mRNA levels of the key genes in the assembly and secretion of VLDL, the concentrations of VLDL and TG were decreased significantly when FMO3 was down-expressed, but it was opposite when FMO3 was overexpressed. This study indicated that FMO3 can regulate the assembly and secretion of VLDL in calf primary hepatocytes, thus regulate the deposition of TG in calf primary hepatocytes.