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Ginsenoside Re Reduces Insulin Resistance through Inhibition of c-Jun NH₂-Terminal Kinase and Nuclear Factor-B

Laboratory of Endocrinology and Metabolism (Z.Z., X.L., Y.S., G.N.), Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Shanghai Jiao Tong University School of Medicine and Shanghai Clinical Center for Endocrine and Metabolic Diseases (Z.Z., X.L., W.L., Y.Y., H.G., J.Y., G.N.), Department of Endocrinology and Metabolism, and Division of Endocrinology and Metabolism (X.L., G.N.), E-Institutes of Shanghai Universities, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China

Address all correspondence and requests for reprints to: Guang Ning, Shanghai Clinical Center for Endocrine and Metabolic Diseases, and Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai 200025, China. E-mail: guangning{at}medmail.com.cn.

Ginsenoside Re (Re), a compound derived from Panax ginseng, shows an antidiabetic effect. However, the molecular basis of its action remains unknown. We investigated insulin signaling and the antiinflammatory effect by Re in 3T3-L1 adipocytes and in high-fat diet (HFD) rats to dissect its anti-hyperglycemic mechanism. Glucose uptake was measured in 3T3-L1 cells and glucose infusion rate determined by clamp in HFD rats. The insulin signaling cascade, including insulin receptor (IR) β-subunit, IR substrate-1, phosphatidylinositol 3-kinase, Akt and Akt substrate of 160 kDa, and glucose transporter-4 translocation are examined. Furthermore, c-Jun NH₂-terminal kinase (JNK), MAPK, and nuclear factor (NF)-B signaling cascades were also assessed. The results show Re increases glucose uptake in 3T3-L1 cells and glucose infusion rate in HFD rats. The activation of insulin signaling by Re is initiated at IR substrate-1 and further passes on through phosphatidylinositol 3-kinase and downstream signaling cascades. Moreover, Re demonstrates an impressive suppression of JNK and NF-B activation and inhibitor of NF-B degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-B activation.

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