Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatotoxic effect of 1,1 bis (p-chlorophenyl) 2,2,2 trichloroethane (DDT) treatment for 10 consecutive days has been examined in Wistar rats. DDT exposure increased relative liver weight, dose dependently, with a marked decrease of glycogen content and profound histological changes including cytoplasmic vacuolization, signs of necrosis and nuclear enlargement. The hepatomegaly induced by DDT (50 and 100 mg/kg body weight day-1) appeared not to be accompanied by a significant alteration of the hepatic glucocorticoid receptor concentration and affinity while, serum corticosteroid binding globulin level increased slightly with the lower dose of the pesticide. It is concluded that a short-term exposure to DDT did not lead to a status stress and, therefore, the hepatotoxic effect of organochlorine seemed not to be mediated by endogenous glucocorticoids.
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PMID:Acute hepatotoxicity of DDT: effect on glucocorticoid receptors and serum transcortin. 1127 8

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.
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PMID:Dexamethasone-induced hepatomegaly and steatosis in larval zebrafish. 2871 4

Excessive or chronic stress can lead to a variety of diseases due to aberrant activation of the glucocorticoid receptor (GR), a ligand activated transcription factor. Pregnancy represents a particular window of sensitivity in which excessive stress can have adverse outcomes, particularly on the developing fetus. Here we show maternal hepatic stress hormone responsiveness is diminished via epigenetic silencing of the glucocorticoid receptor during pregnancy. Provocatively, reinstallation of GR to hepatocytes during pregnancy by adeno-associated viral transduction dysregulates genes involved in proliferation, resulting in impaired pregnancy-induced hepatomegaly. Disruption of the maternal hepatic adaptation to pregnancy results in in utero growth restriction (IUGR). These data demonstrate pregnancy antagonizes the liver-specific effects of stress hormone signaling in the maternal compartment to ultimately support the healthy development of embryos.
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PMID:Silencing of maternal hepatic glucocorticoid receptor is essential for normal fetal development in mice. 3091 79