中文摘要：

糖尿病和骨质疏松之间的关系逐渐成为新的研究热点，但存在很大的争议。循环血液中的高浓度葡萄糖可与体内多种蛋白结合并在胶原组织中形成糖基化终末产物而降低骨强度，又可以通过抑制活性氧的产生及氧化还原敏感性的NF—KB活性，抑制核转录因子-KB受体活化因子配体（RANKL）诱导的破骨细胞形成和骨吸收。糖尿病患者的一系列并发症可以降低骨组织局部营养供应及钙磷摄入，减低肌张力及骨密度，增加骨折的风险。超重或肥胖的2型糖尿病患者又可增加炎症因子、脂联素和瘦素的分泌，促进破骨细胞的形成与分泌，增加骨髓基质干细胞向脂肪细胞分化；另一方面，脂联素和瘦素又可以促进成骨细胞增殖、分化及活性，促进骨形成。笔者将从糖尿病与骨代谢的内在病理生理机制出发，探讨糖尿病对骨代谢的影响。

英文摘要：

The relationship between diabetes and osteoporosis has gradually become a new research hotspot, but is still much controversy. High concentration of blood glucose can be bond to varieties of proteins in vivo and form glycosylation end products in col- lagen tissue and reduce bone strength, besides it can inhibit RANKL induced osteoclast formation and bone resorption by repressing redox-sensitive NF-kappa B activity. A series of diabetes mellitus complications can induce less local bone nutrition supply and calcium and phosphorus sorption, reduce muscle tension and bone mineral density, which leads to the increase of fracture risk. Type 2 diabetes patients with overweight or obesity often have increased secretion of inflammation factors, adiponectin and leptin, which promotes the formation of osteoclasts and encourages bone marrow stromal stem ceils to differentiate into adipocytes; On the other hand, adiponectin and leptin can facilitate osteoblasts proliferation, differentiation and activity, and promotes bone formation. This article will discuss how diabetes works on bone metabolism and the underlying pathophysiological and physiological mechanism.