论文部分内容阅读
Genetic variations confer susceptibility to non-alcoholic fatty liver disease(NAFLD),but the associated genes are largely unknown.In this study,we demonstrate that a slc7a3a-mutant zebrafish can develop hepatic steatosis after the maternally deposited yolk is depleted.The formation of hepatic steatosis is suppressed by adequate nutrition in slc7a3a mutants.Adult mutants exhibited an excess amount of liver neutral lipids and induced expression of hepatic lipid biosynthetic genes under fasting.These phenotypes can be rescued by ectopic expression of wild-type zebrafish slc7a3a or human SLC7A3,indicating the importance of Slc7a3a to the liver energy metabolism under fasting.Silencing the SLC7A3 in L02 cells led to an increase in the oxidative stress(OS)and the activation of OS-associated signaling pathways due to the accumulation of oleic acid(OA)in siSLC7A3-L02 cells.These data suggest that the deficiency in Slc7a3a is involved in the oxidative injury and increased lipid storage.