二甲双胍对骨骼的影响及其分子机制  

Effects of metformin on bone metabolism and its mechanism

作　　者：李毅敏[1] 严孙杰[1] 

机构地区：[1]福建医科大学附属第一医院内分泌科,福州350005

出　　处：《国际内分泌代谢杂志》2010年第4期239-241,共3页International Journal of Endocrinology and Metabolism

基　　金：福建省自然科学基金资助项目（2009J01135）

摘　　要：研究发现二甲双胍可对抗骨量丢失,减少糖尿病患者的骨折风险,其确切机制尚未阐明.目前的研究主要集中于骨髓间充质干细胞和成骨细胞,认为二甲双胍可促进成骨细胞的增殖、分化和矿化,提高碱性磷酸酶（ALP）和Ⅰ型胶原蛋白（Col Ⅰ）的表达和分泌.已有的证据认为二甲双胍可通过AMP活化蛋白激酶（AMPK）通路、细胞外信号调节激酶（ERK）通路及对过氧化物酶体增殖物活化受体γ（PPARγ）/核转录因子α1（Cbfα1）的调控,实现对成骨细胞生物学行为的调节,并具有拮抗高糖毒性的作用.对其进行深入研究,可能为糖尿病患者骨质疏松的防治提供有价值的用药参考.Recent researches indicate that metformin has the role of inhibiting bone loss and reducing the incidence of fractures in patients with diabetes mellitus, but the exact mechanism has not been clarified. Current studies mainly focuses on mesenchymal stem cells and osteoblasts and suggest that metfotmin can promote the proliferation,differentiation and mineralization of osteoblasts,raise the expression and secretion of alkaline phosphatase（ ALP） and type Ⅰ collagen（Col Ⅰ ）. Some existing evidences indicate that metformin regulates the biological behaviour of osteoblasts via activating AMPK/ERK signal pathway, and regulating the expression of PPARγ/Cbfαl ,and it also can resist the deleterious effects of high blood glucose. These researches may provide valuable references to the prevention and treatment of diabetic osteoporosis.

关 键 词：二甲双胍 骨质疏松 成骨细胞 骨髓间充质干细胞 

分 类 号：R965[医药卫生—药理学]