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Genistein alleviates the development of nonalcoholic steatohepatitis in A po E ―/― mice fed a high‐fat diet
Author(s) -
Jeon Sookyoung,
Park YounJin,
Kwon Young Hye
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300112
Subject(s) - medicine , endocrinology , apolipoprotein e , cd36 , steatosis , scavenger receptor , apolipoprotein b , chemistry , steatohepatitis , cholesterol , fatty liver , biology , receptor , lipoprotein , disease
Scope Genistein ( GEN ) is a compound that has been shown to alleviate hepatic steatosis. Here, we investigated its protective effects against non‐alcoholic steatohepatitis ( NASH ) development in apolipoprotein E ‐deficient ( A po E ―/― ) mice fed a high‐fat diet ( HFD ). Methods and results Wild‐type and A po E ―/― mice were fed an HFD with or without GEN (0.5 g/kg diet) for 24 weeks. Body weights were reduced and fecal cholesterol excretion was increased by GEN . GEN supplementation lowered serum and hepatic cholesterol and lipid peroxidation levels, and hepatic heme oxygenase 1 protein levels in A po E ―/― mice. Hepatic expressions of scavenger receptors involved in oxidized LDL uptake, CD 36 and scavenger receptor A , were downregulated by GEN . GEN reduced serum alanine aminotransferase and monocyte chemoattractant protein 1 levels, and hepatic nuclear factor‐κ B ‐mediated inflammatory gene expressions in A po E ―/― mice. These levels were higher in A po E ―/― mice fed an HFD than their corresponding wild‐type mice. GEN also alleviated hepatic steatosis by reducing m RNA levels of monoacylglycerol O ‐acyltransferase 1, a target gene of peroxisome proliferator‐activated receptor γ. Conclusion GEN alleviated NASH as well as hypercholesterolemia and obesity in A po E ―/― mice fed an HFD . Restoration of altered cholesterol metabolism and oxidative stress may be involved in the protective effect of GEN against NASH development.