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Biochanin A improves hepatic steatosis and insulin resistance by regulating the hepatic lipid and glucose metabolic pathways in diet‐induced obese mice
Author(s) -
Park HeeSook,
Hur Haeng Jeon,
Kim SoonHee,
Park SuJin,
Hong Moon Ju,
Sung Mi Jeong,
Kwon Dae Young,
Kim MyungSunny
Publication year - 2016
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.201500689
Subject(s) - medicine , endocrinology , insulin resistance , steatosis , lipogenesis , lipid metabolism , biochanin a , peroxisome proliferator activated receptor , insulin , fatty liver , biology , carbohydrate metabolism , insulin receptor , gluconeogenesis , chemistry , metabolism , receptor , daidzein , disease , genistein
Scope Natural compounds that regulate peroxisome proliferator‐activated receptor alpha (PPARα) have been reported to have beneficial effects in obesity‐mediated metabolic disorders. In this study, we demonstrated that biochanin A (BA), an agonist of PPAR‐α, improved hepatic steatosis and insulin resistance by regulating hepatic lipid and glucose metabolism. Methods and results C57BL/6 mice were fed a normal chow diet, a high‐fat diet (HFD), and an HFD supplemented with 0.05% BA for 12 weeks. Histological and biochemical examinations indicated that BA prevented obesity‐induced hepatic steatosis and insulin resistance in HFD‐fed mice. BA stimulated the transcriptional activation of PPAR‐α in vitro and increased the expression of PPAR‐α and its regulatory proteins in the liver. CE‐TOF/MS analyses indicated that BA administration promoted the recovery of metabolites involved in phosphatidylcholine synthesis, lipogenesis, and beta‐oxidation in the livers of obese mice. BA also suppressed the levels of gluconeogenesis‐related metabolites and the expression of the associated enzymes, glucose 6‐phosphatase and pyruvate kinase. Conclusion Taken together, these results showed that BA ameliorated metabolic disorders such as hepatic steatosis and insulin resistance by modulating lipid and glucose metabolism in diet‐induced obesity. Thus, BA may be a potential therapeutic agent for the prevention of obesity‐mediated hepatic steatosis and insulin resistance.