2008-4-18 13:42:29

Molecular Endocrinology:人参降低血糖机理

上海交通大学附属瑞金医院内分泌代谢病临床医学中心的研究人员日前发现人参皂苷Re是降低血糖的主要成分,并从机理上阐明了人参皂苷Re的降血糖作用机制。这一成果已发表在业内著名的《分子内分泌学》(Molecular Endocrinology)杂志上。

糖尿病在我国古代中医被称为“消渴病”,中医对于消渴病的记载最早见于两千多年前的《黄帝内经》。人参是传统名贵药材,也是现代人用来滋补元气、保健强身的重要滋补佳品。人参皂苷是人参的主要有效成分。到目前为止, 已经从人参中至少分离提取了40多种人参皂苷单体。人参作为治疗糖尿病的重要中药不仅在中医药典籍中早有记载,而且多项现代研究也证明人参及其有效成分人参皂苷具有改善糖尿病症状的作用。

上海交通大学医学院内分泌代谢病临床医学中心研究人员发现,人参中的人参皂苷Re是降低血糖的主要成分,而人参皂苷Re之所以可以降低血糖,是由于它能增强胰岛素的作用,起到“类胰岛素”作用。

人参用来治疗糖尿病虽然有许多益处,但并非百无禁忌。著名内分泌专家、上海交通大学附属瑞金医院副院长宁光教授认为,人参皂苷Re虽然可以降低血糖,但滥用人参治疗糖尿病甚至可能吃出病来。人参性温,适用于寒症,如血压偏高的病人不应轻易服用;人参有抗利尿作用,肾功能不全或者有浮肿的病人不宜使用;感冒发热时一般不宜服用人参等。另外,人参中的红参等在炮制过程会加入糖进行处理,糖尿病病人也不宜多服用。临床上用人参来治疗糖尿病时,应该根据实际情况谨慎选用,并且应在专业医师指导下,根据个人不同病情选择最佳的治疗方法。

此外,研究人员还发现人参的另一成分皂苷Rb1有类似胰岛素增敏剂的作用,从而也具有降低血糖功能。(来源:新华网 仇逸)

生物谷推荐原始出处:

Molecular Endocrinology),doi:10.1210/me.2007-0119,Zhiguo Zhang, Guang Ning

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

Zhiguo Zhang, Xiaoying Li, Wenshan Lv, Yisheng Yang, Hong Gao, Jun Yang, Yun Shen and Guang Ning

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)-{kappa}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-{kappa}B activation and inhibitor of NF-{kappa}B{alpha} degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-{kappa}B activation.

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