Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0015695 (
fatty liver
)
13,941
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Toxic effects of excessive vitamin A and of excessive vitamin ADE were studied in 9 mixed Labrador Retriever pups. Clinical signs were loss of body weight, dullness,
emaciation
, roughened coat, evident pain in limb joints, and retarded growth. Radiologic changes were decreases in overall length and thickness of long bones, development of osteophytes, periosteal reaction, and premature closure of epiphyses. Pathologic changes were degenerative epiphyseal plate, hemorrhage and exostotic proliferation of periosteum,
fatty liver
, and microcalculi in kidney. Toxic effects of excessive vitamin A did not appear to be so great when it was administered as vitamin ADE.
...
PMID:Hypervitaminosis A in the dog. 119 Jun 3
The pathogenesis of
fatty liver
disease remains largely unknown. Here, we assessed the importance of hepatic fat accumulation on the progression of hepatitis in zebrafish by liver specific expression of Hepatitis B virus X protein (HBx). Transgenic zebrafish lines, GBXs, which selectively express the GBx transgene (GFP-fused HBx gene) in liver, were established. GBX Liver phenotypes were evaluated by histopathology and molecular analysis of fatty acid (FA) metabolism-related genes expression. Most GBXs (66-81%) displayed obvious
emaciation
starting at 4 months old. Over 99% of the emaciated GBXs developed
hepatic steatosis
or steatohepatitis, which in turn led to liver hypoplasia. The liver histology of GBXs displayed steatosis, lobular inflammation, and balloon degeneration, similar to non-alcoholic steatohepatitis (NASH). Oil red O stain detected the accumulation of fatty droplets in GBXs. RT-PCR and Q-rt-PCR analysis revealed that GBx induced
hepatic steatosis
had significant increases in the expression of lipogenic genes, C/EBP-alpha, SREBP1, ChREBP and PPAR-gamma, which then activate key enzymes of the de novo FA synthesis, ACC1, FAS, SCD1, AGAPT, PAP and DGAT2. In addition, the steatohepatitic GBX liver progressed to liver degeneration and exhibited significant differential gene expression in apoptosis and stress. The GBX models exhibited both the genetic and functional factors involved in lipid accumulation and steatosis-associated liver injury. In addition, GBXs with transmissible NASH-like phenotypes provide a promising model for studying liver disease.
...
PMID:Increase of hepatic fat accumulation by liver specific expression of Hepatitis B virus X protein in zebrafish. 2041 98
A 49-year-old Japanese woman with polycystic liver disease (PLD) was admitted for right hypochondrial pain. CT showed a huge enhancing mass in the liver. She tested negative for other liver diseases, such as hepatitis B and C and alcoholic liver disease. After the patient expired due to hepatic failure, an autopsy revealed poorly differentiated hepatocellular carcinoma (HCC) surrounded by multiple hepatic cysts. The small amount of residual hepatic parenchyma showed nonalcoholic
fatty liver
disease (NAFLD) with severe steatosis. Severe
emaciation
was also apparent. This case suggests that malnutrition in patients with symptomatic PLD may contribute to the development of HCC via NAFLD.
...
PMID:Hepatocellular Carcinoma in a Patient with Polycystic Liver Disease. 2623 31