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The fruit of Acanthopanax senticosus (Rupr. et Maxim) Harms improves insulin resistance and hepatic lipid accumulation by modulation of liver AMP-activated protein kinase activity and lipogenic gene expression in high-fat-diet-fed obese mice

Abstract Obesity-associated insulin resistance is a major risk factor for most metabolic diseases, including dyslipidemia and type 2 diabetes. Acanthopanax senticosus (Rupr. et Maxim) Harms (Goka) root has been used in traditional Chinese Medicine for treatment of diabetes and other conditions; howe...

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Published in:Nutrition research (New York, N.Y.) N.Y.), 2016
Main Authors: Saito, Tetsuo, Nishida, Miyako, Saito, Masafumi, Tanabe, Akari, Eitsuka, Takahiro, Yuan, Shi-Hua, Ikekawa, Nobuo, Nishida, Hiroshi
Format: Article
Language:English
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Summary:Abstract Obesity-associated insulin resistance is a major risk factor for most metabolic diseases, including dyslipidemia and type 2 diabetes. Acanthopanax senticosus (Rupr. et Maxim) Harms (Goka) root has been used in traditional Chinese Medicine for treatment of diabetes and other conditions; however, little is known about the effects of Goka fruit (GF). GF is rich in anthocyanin, which has beneficial effects on obesity and insulin resistance via activation of AMP-activated protein kinase (AMPK). We hypothesized that GF can improve obesity-associated insulin resistance. The aim of the present study was to investigate whether GF improves insulin resistance in high-fat diet (HFD)-induced obese mice. HFD mice treated with GF (500 mg/kg and 1000 mg/kg) for 12 weeks showed an improved glucose tolerance and insulin sensitivity, as well as reduced plasma insulin, and liver lipid accumulation. Moreover, GF administration to HFD mice resulted in downregulation of fatty acid synthase expression and upregulation of cholesterol 7-alpha-hydroxylase expression in the liver. Notably, AMPK phosphorylation in the liver increased after GF administration. In summary, GF supplementation improved obesity-associated insulin resistance and hepatic lipid accumulation through modulation of AMPK activity and lipid metabolism-associated gene expression.
ISSN:0271-5317
DOI:10.1016/j.nutres.2016.09.004