噻唑烷二酮类药物对骨代谢的影响

噻唑烷二酮类（TZDs）药物是核转录因子过氧化物酶体增殖物激活受体γ（PPARγ）的激动剂,是临床上常用的胰岛素增敏剂,用来治疗2型糖尿病等存在胰岛素抵抗的疾病。近年发现TZDs增加女性骨折的危险性。体外及动物实验证实TZDs促进间充质干细胞向脂肪细胞系分化,而抑制其向成骨细胞系分化,减少骨形成,还可能具有促进破骨细胞分化、增加骨吸收的作用,从而导致骨量减少。TZDs还可能通过改变某些激素和细胞因子的水平间接地影响骨代谢。     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物肾脏保护作用研究进展

噻唑烷二酮类(TZDs)药物为过氧化物酶体增殖物活化受体(PPAR)γ激动剂,是一类通过胰岛素增敏作用来治疗2型糖尿病的药物.研究表明,肾脏系膜细胞、肾小管细胞及足细胞上均存在PPART.越来越多的动物及临床证据支持TZDs药物可以通过改善肾脏血流动力学和内皮功能、抗糖基化、抑制炎性反应、氧化应激等多种机制来延缓肾脏衰竭.发挥直接的肾脏保护作用.且不依赖于改善糖、脂代谢,降低高胰岛素血症的全身作用.因此,为糖尿病肾病及其他慢性肾病的药物治疗提供了新的思路和方法.     

噻唑烷二酮类药物不良反应的再认识

噻唑烷二酬类药物(TZDs)通过激活过氧化物酶体增殖物活化受体-γ,增加外周组织对胰岛素的敏感性而改善胰岛素抵抗,以其独特的作用机制在口服抗糖尿病药物中独树一帜.然而,近年来有关TZDs不良反应的报道日渐增多.在肝毒性、体重增加、水肿、心力衰竭等不良反应得到确认的同时,关于其心血管与骨代谢方面的不良反应更是备受关注.科学面合理地分析与认识这些不良反应,对指导临床实践具有重要意义.     

糖尿病对骨量的影响及其相关因素的分析

为评估糖尿病对骨量的影响及各种相关因素对骨丢失的意义，本文对３００例糖尿病患者和１８００例正常人的前臂进行了骨密度测定。根据骨密度结果的不同，在骨量正常和降低组间进行了有关因素的比较，对可能影响骨量的各种因素进行了逐步回归分析。结果为：糖尿病人骨量减少的发生率为５８％。Ⅰ型和Ⅱ型糖尿病骨量减少的发生率和程度无显著性差异。骨量减少的发生率与病程长短无关。血碱性磷酸酶和尿羟脯氨酸在骨密度降低组显著增高，可作为观察骨量减少较为敏感的两项生化指标。多因素逐步回归分析结果所分析的指标对骨量无显著影响。由于病程对骨量减少无明显影响，我们认为骨量减少有可能是糖尿病基础病变的一部分。胰岛素缺乏所导致的骨形成不足和骨重建负平衡可能为骨量减少的原因。若给予足量的胰岛素治疗对预防和减轻骨量减少是有效的。     

噻唑烷二酮类药物的抗肿瘤作用

噻唑烷二酮（TZDs）是用于治疗以胰岛素抵抗为特征的2型糖尿病的药物。它主要通过作用于核受体家族中的过氧化物酶增殖体的激活受体γ（PPARγ）来发挥抗糖尿病的作用。近年来,越来越多的实验证据发现其具有一定的抗肿瘤作用,涉及的机制主要有诱导细胞周期的终止,促进细胞的凋亡或分化,抑制肿瘤的转移及血管新生等。     

噻唑烷二酮类药物与糖尿病肾病关系的研究进展

噻唑烷二酮(TZDs)是一类通过改善胰岛素敏感性降低血糖的经典药物。动物实验和临床研究证实TZDs除了通过降低血胰岛素和血糖水平之外,尚可通过抗炎、调节脂质紊乱、改善内皮等多种途径防治糖尿病肾病。     

噻唑烷二酮类药物对脂肪细胞增殖与分化的影响及其临床应用

目的研究噻唑烷二酮类代表药物曲格列酮对人大网膜前脂肪细胞增殖和分化的影响及其临床应用意义。方法体外培养人大网膜前脂肪细胞,曲格列酮作用后,四唑盐(MTT)比色法观察细胞增殖;油红O染色抽提法观察细胞分化。结果浓度为1μmol/L,10μmol/L曲格列酮能够明显促进前脂肪细胞的增殖,同时也促进前脂肪细胞向脂肪细胞分化。结论噻唑烷二酮类药物促进前脂肪细胞成熟,发挥脂肪组织完善的储脂和内分泌功能,改善胰岛素抵抗状态。在临床上,对于以胰岛素抵抗为基础的糖尿病和动脉粥样硬化等疾病应作为基础用药。     

体重及其构成成分对2型糖尿病患者骨量的影响

目的探讨体重及其构成成分对2型糖尿病（T2DM）患者骨量的影响。方法DEXA测定131例T2DM患者及89名对照者的瘦体重、总体脂量、全身脂肪含量、全身骨密度（BMD）及骨矿含量（BMC）,计算BMI、校正骨矿含量（CBMC）,对比两组上述指标,分析体重及其构成成分与骨量关系。结果T2DM组体重、瘦体重及BMC大于对照组,两组间BMD、CBMC无差异。在T2DM组成员中,体重、瘦体重、总体脂量与骨量呈正相关,全身脂肪含量与骨量呈负相关。结论T2DM患者骨密度与正常人比较无下降,较高的体重、瘦体重及总体脂量是其骨量保护因素,瘦体重的保护作用更显著。     

中等强度跑台运动对去卵巢大鼠后肢骨骨量和脂质含量的影响

目的 观察中等强度跑台运动对去卵巢大鼠后肢骨骨量及脂质含量的影响.方法 40只雌性3月龄SD大鼠按体重随机分为假手术组、去卵巢静止组、去卵巢运动组和雌激素组,每组10只.实验结束时,双能X线骨密度仪检测游离股骨和胫骨的骨密度(BMD)和骨矿物含量(BMC),乙醇/氯仿提取股骨远端及胫骨近端总胆固醇(TC)和甘油三酯(TG).结果 (1)与假手术组相比,去卵巢静止组大鼠股骨远端(P＜0.05)及胫骨近端(P ＜0.01)BMD和BMC显著下降,而股骨远端Tc(P＜0.05)、TG(P ＜0.01)和胫骨近端TG(P＜0.01)显著升高;(2)与去卵巢静止组相比,去卵巢运动组和雌激素组股骨远端及胫骨近端BMD和BMC显著升高(P＜0.05),去卵巢运动组大鼠股骨远端TG(P ＜0.01)、雌激素组大鼠股骨远端TC(P＜0.05)、TG(P＜0.01)和胫骨近端TG(P＜0.o1)显著降低.结论 中等强度跑台运动能显著抑制去卵巢大鼠后肢骨骨量的减少和脂质含量的增加.