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目的 探讨晚期糖化终末产物 (AGE)在糖尿病骨质疏松发病中的作用。方法 用链脲佐菌素制做糖尿病大鼠模型 ,3个月后测定大鼠腰椎骨密度及骨胶原中 AGE的含量及观察血、尿生化指标的变化。结果 糖尿病大鼠骨胶原中 AGE的含量与正常对照组相比明显升高 (P<0 .0 0 1 ) ,而骨密度明显降低 (P<0 .0 2 )。 2 4 h尿钙增加 ,血钙降低。结论 糖尿病大鼠骨胶原中 AGE含量的增加所导致的成骨作用降低 ,可能是糖尿病骨质疏松发病的主要原因。
Objective To investigate the role of advanced glycation end products (AGE) in the pathogenesis of diabetic osteoporosis. Methods Diabetic rats were induced by streptozotocin. The bone mineral density (BMD) of lumbar vertebrae, the content of AGE in bone collagen and the changes of blood and urine biochemical parameters were measured 3 months later. Results Compared with the normal control group, the content of AGE in diabetic rats increased significantly (P <0.01), while the BMD decreased significantly (P <0. 02). 2 4 h increased urinary calcium, decreased serum calcium. Conclusion The decreased osteogenesis induced by the increase of AGE in the collagen of diabetic rats may be the main reason for the pathogenesis of diabetic osteoporosis.