Abstract Title:

Genistein improves liver function and attenuates non-alcoholic fatty liver disease in a rat model of insulin resistance.

Abstract Source:

J Diabetes. 2009 Dec;1(4):278-87. Epub 2009 Jul 21. PMID: 20923528

Abstract Author(s):

Sumiyabanu Mohamed Salih, Palanisamy Nallasamy, Pooranaperundevi Muniyandi, Viswanathan Periyasami, Anuradha Carani Venkatraman

Article Affiliation:

Department of Biochemistry and Biotechnology, Rajah Muthiah Medical College, Annamalai University, Annamalai Nagar, Tamil Nadu, India.


BACKGROUND: The high fructose-fed rat is widely used as a model of insulin resistance. Genistein, a soy isoflavone, has been shown to improve insulin sensitivity in this model. The present study investigated whether genistein could prevent fatty liver disease in this model.

METHODS: Male Wistar rats were fed a diet containing starch (control) or 60% fructose (insulin-resistant model). Fifteen days later, rats in each dietary group were divided into two groups and were treated with either genistein (1 mg/kg per day) in dimethylsulfoxide (DMSO) or 30% DMSO alone. After 60 days, markers of liver injury, oxidative stress, interleukin (IL)-6, tumor necrosis factor (TNF)-α, lipids, lipoprotein profile, nitrite, and nitrosothiol in the plasma and liver were quantified. Liver sections were examined for 3-nitrotyrosine (3-NT) expression and pathological lesions.

RESULTS: Fructose-fed rats displayed hyperlipidemia, significant changes in plasma lipoprotein profile, and increases in IL-6 and TNF-α levels compared with control. In addition, the accumulation of lipids, liver injury, a decline in liver function, inactivation of the glyoxalase system, depletion of antioxidants, and increased 3-NT expression were observed in the fructose-fed group. Administration of genistein to fructose-fed rats significantly reduced these biochemical and histological abnormalities.

CONCLUSIONS: Genistein activates the antioxidant profile, decreases IL-6 and TNF-α concentrations, prevents oxidative damage, and ameliorates fatty liver in insulin-resistant rats.

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