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中国科学院大学学报 ›› 2007, Vol. 24 ›› Issue (2): 217-222.DOI: 10.7523/j.issn.2095-6134.2007.2.012

• 论文 • 上一篇    下一篇

STZ诱导的糖尿病对骨密度和血清睾酮的影响(英文)

费聿荣 韦 单 李 明 张 敏 张晓琳 丁文军 杨建虹   

  1. 中国科学院研究生院 生物系 北京 100049
  • 收稿日期:1900-01-01 修回日期:1900-01-01 发布日期:2007-03-15

Effect of STZ-induced diabetes on bone mineral density and testosterone

FEI Yu-Rong, WEI Dan, LI Ming, ZHANG Min, ZHANG Xiao-Lin, DING Wen-Jun, YANG Jian-Hong   

  1. Department of Biology, Graduate University of Chinese Academy of Sciences, 19 Yuquan Road, Beijing 100049, P. R. China
  • Received:1900-01-01 Revised:1900-01-01 Published:2007-03-15

摘要: 目的:探讨链脲霉素(STZ)诱导的糖尿病对大鼠骨代谢的影响及机制。材料与方法:雄性Wistar大鼠随机分成3组: 正常组(n = 6),糖尿病组(n = 5)和胰岛素治疗糖尿病组 (n = 5)。大鼠尾静脉一次性注射STZ(50 mg/kg 体重),选择空腹12 h血糖大于12 mmol/L的大鼠为本实验所需的糖尿病模型。治疗组大鼠每天在同一时间给予1.8-2.2U的胰岛素。实验周期为持续32天。采用双能X线骨吸收法(DEXA)测定股骨密度,ELISA法测定血清雄性激素睾酮水平,生化分析仪测定血清碱性磷酸酶、钙、磷浓度。结果:糖尿病大鼠的股骨密度和血清睾酮均显著低于正常组(P < 0.01),血清总碱性磷酸酶明显高于正常组和胰岛素治疗组(P < 0.01)。三组之间血钙和血磷的水平无明显差异。胰岛素治疗后糖尿病大鼠的骨密度、血清睾酮与总碱性磷酸酶得到明显的改善。结论:糖尿病严重影响骨密度,胰岛素缺乏及雄性激素降低是导致糖尿病性骨质疏松重要原因。胰岛素治疗能预防骨流失和提高血清睾酮浓度。

关键词: 骨质疏松, 糖尿病, 骨密度, 睾酮

Abstract: Objective: To investigate the effect of diabetes mellitus on bone metabolism, bone mineral density (BMD) and serum testosterone were studied in STZ-induced diabetic male rats. Materials and methods: Male Wistar rats were randomly divided into control group (n = 6), diabetic group (n = 5) and insulin-treated diabetic group (n = 5). Diabetes was intravenously induced by injection of streptozotocin (STZ, 50 mg/kg body weight), confirmed by 12 h fasting blood glucose concentration (12 mmol/L). The treatment group was subcutaneously injected with protamine zinc insulin (1.8-2.2U/animal) at the same time every day. The experiment lasted 32 days. Femoral BMD was determined by dual-energy X-ray absorptiometry (DEXA). Serum testosterone was detected by Enzyme-linked Immunosorbent Assay (ELISA) kit. Total alkaline phosphatase (ALP), calcium (Ca) and phosphorus (P) in serum were measured by bio-machine. Results: Femoral BMD in diabetic group was significantly lower than that in control (P < 0.01) but reserved by insulin treatment. Testosterone in serum was also reduced in diabetic rats (P < 0.01) and normalized by insulin treatment. Serum ALP concentration was markedly higher in diabetics (P < 0.01) compared to the controls and prevented by insulin treatment. However, no significant differences were observed in serum Ca and P among three groups. Conclusion: BMD is seriously affected by diabetes. Insulin deficiency and testosterone decrease are important causes of diabetic osteoporosis. And insulin treatment preserved bone loss and testosterone depression.

Key words: Osteoporosis, Diabetes Mellitus, Bone Mineral Density, Testosterone

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