抄録
Fish hepatobiliary syndrome, characterized by fatty liver and hepatomegaly, has been frequently reported in many cultured fish species and caused dramatic loss in China. Glucocorticoid is hypothesized to be an important non-nutritional factor for hepatomegaly and fatty liver development in fish. The present study aimed to establish a dexamethasone-induced zebrafish model of fatty liver and hepatomegaly and investigate the role of glucocorticoid receptor (GR) and RU 486 (a glucocorticoid antagonist) in hepatomegaly and fatty liver development. Exposure of larval zebrafish (5 dpf) to dexamethasone for 48h caused significant increases of liver size and number of fish with hepatic steatosis. The increase of liver size by dexamethasone was significantly reversed by treatment with RU 486 and gene knock-down with morpholino to GR, the dexamethasone-induced hepatic steatosis was significantly inhibited by treatment with RU 486. The gene expression analysis showed that dexamethasone upregulated Angptl4 and downregulated CYP3A. Overall, we demonstrated that dexamethasone induced zebrafish hepatomegaly and fatty liver, which is possibly mediated by GR.
