晚期糖化终末产物在老年大鼠骨质疏松发病中的作用

Effects of advanced glycosylation end products in pathogenesis of senile osteoporosis

目的 探讨晚期糖化终末产物 ( AGE)在老年大鼠骨质疏松发病中的作用。方法 选用 2 0月龄老年大鼠和 3月龄大鼠 ,测定其骨密度及骨胶原中晚期糖化终末产物的含量及血、尿生化指标。结果 老年大鼠骨密度明显低于 3月龄大鼠 ( P<0 .0 5) ,而骨胶原中晚期糖化终末产物的含量明显升高( P<0 .0 0 1)。同时发现老龄组大鼠血清甲状旁腺激素 ( PTH)明显升高 ( P<0 .0 5) ,尿钙与肌酐比值升高( P<0 .0 2 ) ,而尿磷与肌酐比值降低 ( P<0 .0 5)。结论 骨胶原中随年龄增加的晚期糖化终末产物 ,通过多种途径导致骨形成降低 ,骨吸收相对增加而致骨密度下降。 PTH升高并非低血钙引起 ,而与

Objective\ To explore the effects of advanced glycosylation end products (AGEs) in the pathogenesis of senile osteoporosis. Methods\ twenty\|month\|old rats and three\|month\|old rats were used in this study.Bone mineral density,content of AGEs in bone collagen,and serum and urine biochemical indexes were defermined. Results\ The content of AGEP in senile rat bone collagen was higher than that in young group ( P <0.001).Compared with the young group,lumbar bone mineral density in the senile rats was significantly reduced ( P <0.05),serum levels of parathyroid hormone (PTH) significautly increased ( P <0.05),and urine Ca/Cr levels remarkably increased (\%P\%<0.02). Conclusion\ Contents of AGEs in senile rat bone collagen increase with age,which results in absolute reduction of bone formation and relative increase of bone resorption by multiple ways.Increased serum PTH is not a compensatory response to hypocalcemia,but is related to increased AGEs in bone collagen.