2型糖尿病大鼠骨折愈合障碍与体内晚期糖基化终末产物的变化

背景：近年来，晚期糖基化终末产物在骨组织领域的作用日益受到重视，而糖代谢紊乱是引起晚期糖基化终末产物增加的主要原因之一。 目的：观察2型糖尿病大鼠体内晚期糖基化终末产物表达的变化，并探讨其与糖尿病骨折愈合障碍的关系。方法：30只SD大鼠随机均分为2组，实验组制备2型糖尿病模型，对照组正常饲养。糖尿病模型制备成功后，所有大鼠建立左胫骨骨折牵引成骨模型，胫骨延长0.3 mm/d，持续14 d。 结果与结论：牵引结束后，X 射线摄片显示实验组糖尿病模型大鼠骨折断端之间牵引骨痂形成较对照组明显减少；骨痂组织学检查表现为微骨柱排列紊乱，初始基质前沿浅染。ELISA 法检测实验组血清和双侧骨痂组织中晚期糖基化终末产物水平较对照组明显升高（P 〈0.01），骨钙素明显降低（P 〈0.01）。提示2型糖尿病大鼠骨折牵引骨痂生成障碍，而骨组织中晚期糖基化终末产物水平增高可能是导致2型糖尿病骨折愈合障碍的原因。

Impaired fracture healing and change of advanced glycation end products in vivo in type 2 diabetes rats

BACKGROUND：Increasing attention has been paid on the role of advanced glycation end products in bone tissue. Glucose metabolic disorder is one of the main reasons for the increase of advanced glycation end products. OBJECTIVE：To observe the change of advanced glycation end products expressed in type 2 diabetes rats, and to investigate the relationship between impaired fracture healing and change of advanced glycation end products expression in vivo. METHODS：Thirty Sprague-Dawley rats were randomly and equal y divided into two groups：control group （normal feeding） and experimental group （high fat and sucrosum diet feeding to establish type 2 diabetes model）. After diabetes models were established, the model of distraction osteogenesis in the left tibiae of al the rats was produced. Distraction was given 0.3 mm per day and continued for 14 days. RESULTS AND CONCLUSION：After the traction was complete, cal us formation in distraction gap was obviously reduced in experimental group compared with control group by X-ray examination. The array of microcolumn formation was disordered and the area of primary matrix front was catachromasis by histology examination. The enzyme-linked immunosorbent assay results showed that, the level of advanced glycation end products was obviously elevated （P〈0.01） while osteocalcin was obviously reduced （P〈0.01） in experimental group in comparison with control group. The formation of distraction cal us was impaired in the process of fracture healing and blood of type 2 diabetes rats. The increase of advanced glycation end products may be one of the reasons that cause impaired fracture healing in diabetic rats.