Dexamethasone-induced hepatomegaly and steatosis in larval zebrafish

Fish hepatobiliary syndrome, characterized by hepatomegaly and fatty liver, has been frequently reported in many cultured fish species and has caused a dramatic economic loss in China. Glucocorticoids are thought to be important non-nutritional factors for hepatomegaly and fatty liver development. I...

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Published in:Journal of toxicological sciences 2017/08/01, Vol.42(4), pp.455-459
Main Authors: Yin, Guojun, Cao, Liping, Du, Jinliang, Jia, Rui, Kitazawa, Takio, Kubota, Akira, Teraoka, Hiroki
Format: Article
Language:English
Subjects:
Animals
Danio rerio
Dexamethasone
Dexamethasone - toxicity
Disease Models, Animal
Fatty liver
Fatty Liver - chemically induced
Fatty Liver - drug therapy
Fatty Liver - genetics
Fertilization
Gene Knockdown Techniques
Glucocorticoid
Glucocorticoids
Glucocorticoids - toxicity
Hepatomegaly
Hepatomegaly - chemically induced
Hepatomegaly - drug therapy
Hepatomegaly - genetics
Liver
Liver diseases
Mifepristone - pharmacology
Mifepristone - therapeutic use
Receptors, Glucocorticoid - antagonists & inhibitors
Receptors, Glucocorticoid - genetics
Receptors, Glucocorticoid - physiology
Steatosis
Time Factors
Zebrafish
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Summary:Fish hepatobiliary syndrome, characterized by hepatomegaly and fatty liver, has been frequently reported in many cultured fish species and has caused a dramatic economic loss in China. Glucocorticoids are thought to be important non-nutritional factors for hepatomegaly and fatty liver development. In the present study, a dexamethasone-induced zebrafish model of fatty liver and hepatomegaly was established, and the role of glucocorticoid receptor (GR) in the development of hepatomegaly and fatty liver was investigated using developing zebrafish. Exposure of larval zebrafish at 5 days post fertilization (dpf) to dexamethasone for 24 hr caused significant increases of liver size and number of fish with hepatic steatosis at 6 dpf. The increase of liver size caused by dexamethasone was significantly reversed by treatment with RU486, a GR antagonist, and by gene knock-down with a morpholino against the GR. The dexamethasone-induced hepatic steatosis was also inhibited by treatment with RU486. Overall, the results highlight larval zebrafish as a useful model for stress-induced liver failure.
ISSN:0388-1350
1880-3989
DOI:10.2131/jts.42.455