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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 AGE升高有关
Objective To investigate the role of advanced glycation end products (AGE) in the pathogenesis of osteoporosis in aged rats. Methods 20-month-old rats and 3-month-old rats were selected for determination of their bone mineral density, advanced glycation end products and the biochemical markers of blood and urine. Results The bone density of aged rats was significantly lower than that of 3-month-old rats (P <0.05), while the content of advanced glycation end products in collagen was significantly increased (P <0.01). At the same time, the serum PTH was significantly increased (P <0.05), the ratio of urinary calcium to creatinine was increased (P <0. 02), while the ratio of urine P to creatinine was decreased P <0. 05). Conclusions The advanced glycation end products of collagen with age increase the bone formation through a variety of pathways and decrease the bone mineral density with relative increase of bone resorption. PTH is not caused by hypocalcemia, but with elevated AGE