...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Endocrinology >Effects of parathyroid hormone on bone mass, bone strength, and bone regeneration in male rats with type 2 diabetes mellitus
【24h】

Effects of parathyroid hormone on bone mass, bone strength, and bone regeneration in male rats with type 2 diabetes mellitus

机译：甲状旁腺激素对雄性2型糖尿病大鼠骨质量，骨强度和骨再生的影响

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Type 2 diabetes mellitus (T2DM) is associated with increased skeletal fragility and impaired fracture healing. Intermittent PTH therapy increases bone strength; however, its skeletal and metabolic effects in diabetes are unclear.Weassessed whether PTH improves skeletal and metabolic function in rats with T2DM. Subcritical femoral defects were created in diabetic fa/fa and nondiabetic +/+ Zucker Diabetic Fatty (ZDF) rats and internally stabilized. Vehicle or 75 μg/kg/d PTH(1-84) was sc administered over 12 weeks. Skeletal effects were evaluated by μCT, biomechanical testing, histomorphometry, and biochemical markers, and defect regeneration was analyzed by μCT. Glucose homeostasis was assessed using glucose tolerance testing and pancreas histology. In diabetic rats, bone mass was significantly lower in the distal femur and vertebrae, respectively, and increased after PTH treatment by up to 23% in nondiabetic and up to 18% in diabetic rats (P < .0001). Diabetic rats showed 23% lower ultimate strength at the spine (P < .0005), which was increased by PTH by 36% in normal and by 16% in diabetic rats (P < .05). PTH increased the bone formation rate by 3-fold in normal and by 2-fold in diabetic rats and improved defect regeneration in normal and diabetic rats (P < .01). PTH did not affect serum levels of undercarboxylated osteocalcin, glucose tolerance, and islet morphology. PTH partially reversed the adverse skeletal effects of T2DM on bone mass, bone strength, and bone defect repair in rats but did not affect energy metabolism. The positive skeletal effects were generally more pronounced in normal compared with diabetic rats.
机译：2型糖尿病（T2DM）与骨骼脆弱性增加和骨折愈合不良有关。间歇性PTH治疗可增强骨骼强度;然而，尚不清楚其在糖尿病中的骨骼和代谢作用。评估PTH是否能改善T2DM大鼠的骨骼和代谢功能。亚临界股骨缺损在糖尿病fa / fa和非糖尿病+ / +祖克糖尿病脂肪（ZDF）大鼠中产生，并且内部稳定。在12周内皮下注射媒介物或75μg/ kg / d PTH（1-84）。通过μCT，生物力学测试，组织形态计量学和生化标志物评估骨骼作用，并通过μCT分析缺损的再生。使用葡萄糖耐量测试和胰腺组织学评估葡萄糖稳态。在糖尿病大鼠中，股骨远端和椎骨的骨量分别显着降低，在非糖尿病患者中，PTH治疗后增加了23％，在糖尿病大鼠中增加了18％（P <.0001）。糖尿病大鼠的脊柱极限强度降低了23％（P <.0005），正常人的PTH增加了36％，糖尿病大鼠的PTH增加了16％（P <.05）。 PTH在正常大鼠和糖尿病大鼠中使骨骼形成率分别提高了3倍和2倍，并改善了正常和糖尿病大鼠的缺损再生（P <.01）。 PTH不会影响血清中羧基不足的骨钙素水平，葡萄糖耐量和胰岛形态。 PTH可部分逆转T2DM对大鼠骨量，骨强度和骨缺损修复的不利骨骼作用，但不影响能量代谢。与糖尿病大鼠相比，在正常情况下，骨骼的积极作用通常更为明显。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号