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Effects of calycosin against high‐fat diet‐induced nonalcoholic fatty liver disease in mice
Author(s) -
Duan Xingping,
Meng Qiang,
Wang Changyuan,
Liu Zhihao,
Sun Huijun,
Huo Xiaokui,
Sun Pengyuan,
Ma Xiaodong,
Peng Jinyong,
Liu Kexin
Publication year - 2018
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.13884
Subject(s) - nonalcoholic fatty liver disease , calycosin , endocrinology , medicine , adiponectin , oil red o , insulin , glycogen , fatty liver , phosphoenolpyruvate carboxykinase , insulin resistance , biology , biochemistry , adipose tissue , adipogenesis , enzyme , daidzein , disease , formononetin , genistein
Background and Aim Nonalcoholic fatty liver disease (NAFLD) has become a major health concern worldwide. The present study was designed to investigate the effects of calycosin against high‐fat diet (HFD)‐induced NAFLD in mice. Methods C57BL/6 J male mice were fed with HFD to induce NAFLD model and treated with or without calycosin for 12 weeks. The levels of ALT, AST, insulin, and adiponectin were measured using biochemical methods. Hemotoxylin and eosin staining and Oil Red O staining were used to determine the liver histopathology changes and measure the degree of lipid accumulation respectively. Glucose tolerance tests and insulin tolerance tests were performed followed by quantitative insulin sensitivity check index determination. Western blot and quantitative real‐time polymerase chain reaction were used to explore the potential mechanism involved in the beneficial effects of calycosin. Results Calycosin effectively decreased the levels of ALT and AST, increased the levels of adiponectin and insulin. Hemotoxylin and eosin staining indicated calycosin treatment remarkably improved liver injury. Oil Red O staining indicated calycosin treatment remarkably improved lipid accumulation. Quantitative insulin sensitivity check index in HFD fed mice was significantly lower than in the standard chow fed mice. Further, calycosin suppressed phosphoenolpyruvate carboxykinase, glucose‐6‐phosphatase, sterol‐regulatory element binding protein 1c, and FASN involved in gluconeogenesis and triglyceride synthesis. Calycosin increased glycogen synthase kinase 3 beta, glucose transporter 4, and phosphorylated insulin receptor substrates 1 and 2 expressions involved in glucose metabolism. The aforementioned beneficial effects of calycosin against HFD‐induced NAFLD may be attributed to farnesoid X receptor activation. Conclusion Calycosin could produce the favorable effects against HFD‐induced NAFLD in mice.