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Inhibitory effect of genistein on nonalcoholic fatty liver disease development in ApoE −/− mice fed a high‐fat diet
Author(s) -
Kwon Young Hye,
Jeon Sookyoung,
Park YounJin
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.862.29
Subject(s) - genistein , medicine , endocrinology , apolipoprotein e , steatosis , fatty liver , steatohepatitis , nonalcoholic fatty liver disease , cholesterol , chemistry , disease
Non‐alcoholic fatty liver disease (NAFLD) occurs in a wide variety of clinical presentations, ranging from asymptomatic hepatic steatosis to severe non‐alcoholic steatohepatitis (NASH). Recent studies reported that ApoE −/− mice fed a high‐fat diet (HFD) can be used as a model of NASH as well as arteriosclerosis. Because genistein has been shown to alleviate hepatic steatosis, we investigated the effects of genistein on the development of NASH in ApoE −/− mice. Both wildtype and ApoE −/− mice were fed either an HFD or an HFD supplemented with genistein (0.5 g/kg diet). After 24 weeks on an HFD, serum triglyceride, total cholesterol, and oxidized lipid levels were more exacerbated in ApoE −/− mice compared to wildtype mice. In addition, ApoE −/− mice exhibited higher serum monocyte chemoattractant protein 1 (MCP‐1) and alanine aminotransferase levels. Cholesterol levels in both serum and liver were alleviated by genistein in ApoE −/− mice. Furthermore, ApoE −/− mice exhibited a reduced serum MCP‐1 levels and hepatic pro‐inflammatory gene expressions (MCP‐1 and cyclooxygenase‐2) in response to genistein. In conclusion, genistein alleviated metabolic abnormalities including hypercholesterolemia and NASH in ApoE −/− mice fed an HFD. Moreover, our findings confirmed that the ApoE −/− mice fed an HFD is a promising long term NASH model. This work was supported by National Research Foundation of Korea.