Longitudinal analysis of murine steatohepatitis model induced by chronic exposure to high-fat diet
| Autor: | Makoto Ito, Jun Suzuki, Takashi Shirakura, Akane Ishihara, Akira Gomori, Masahiko Ito, Hiroyasu Hirose, Hisashi Iwaasa, Minoru Sasaki, Akio Kanatani, Shigeharu Tsujioka |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
medicine.medical_specialty
Hepatology biology CD36 nutritional and metabolic diseases Glutathione medicine.disease digestive system diseases chemistry.chemical_compound Fatty acid synthase Infectious Diseases Endocrinology chemistry Catalase Internal medicine medicine biology.protein Hyperinsulinemia Tumor necrosis factor alpha Steatohepatitis Type I collagen |
| Zdroj: | Hepatology Research. 37:50-57 |
| ISSN: | 1386-6346 |
| DOI: | 10.1111/j.1872-034x.2007.00008.x |
| Popis: | Several lines of epidemiological evidence have suggested that non-alcoholic steatohepatitis (NASH) is closely associated with obesity in humans. However, the precise mechanisms of the progression of NASH and its key metabolic abnormalities remain to be elucidated. We found that long-term high-fat diet (HFD) exposure induces NASH, with excess body weight, hyperinsulinemia and hypercholesteremia in mice. Longitudinal analysis of the model showed that steatohepatitis was induced after onset of metabolic abnormalities. In addition, we found that expression of MCP-1 mRNA was induced in the liver before induction of TNFalpha and type I collagen alpha1 mRNAs, and prior to onset of steatohepatitis. We confirmed that hepatic MCP-1 contents were increased in mice fed HFD for 50 weeks, although the precise role of MCP-1 in the development of NASH remains to be addressed. The mouse model was also characterized by moderate reductions in catalase activity and glutathione content, as well as by overexpression of fatty acid synthase, acetyl-CoA carboxylase 1 and FAT/CD36 mRNAs in the liver. The murine NASH model apparently mimics clinical aspects of the condition and provides insight into NASH. |
| Databáze: | OpenAIRE |
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