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Cited by 253

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Longitudinal analysis of murine steatohepatitis model induced by chronic exposure to high‐fat diet

Ito, Makoto, Suzuki, Jun, Tsujioka, Shigeharu, Sasaki, Minoru, Gomori, Akira, Shirakura, Takashi, Hirose, Hiroyasu, Ito, Masahiko, Ishihara, Akane, Iwaasa, Hisashi, Kanatani, Akio·2007·Hepatology Research

Abstract

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 TNFα and type I collagen α1 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.

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Crossref · 10.1111/j.1872-034x.2007.00008.x

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Metadata

Authors
Ito, M., Suzuki, J., Tsujioka, S., Sasaki, M., Gomori, A., Shirakura, T., Hirose, H., Ito, M., Ishihara, A., Iwaasa, H., & Kanatani, A.
Venue
Hepatology Research
Publisher
Wiley
Published
2007-01
Volume
37
Issue
1
Pages
50-57
ISSN
  • 1386-6346 (ISSN-L)
  • 1872-034X
OpenAlex
W1699654400
Cited by
253
References
8
FWCI
2.93
Type
journal article
Language
en
Open access
closed

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