Department of Epidemiology and Biostatistics, University of California, San Francisco, 185 Berry Street, Suite 5700, San Francisco, CA 94107, USA.
PPAR Res. 2006;2006:24502. doi: 10.1155/PPAR/2006/24502.
Evidence from rodent and in vitro models suggests that activation of PPAR-gamma by thiazolidinediones (TZDs) causes increased bone marrow adiposity and decreased osteoblastogenesis, resulting in bone loss. TZDs are prescribed for the treatment of diabetes, providing an opportunity to determine whether PPAR-gamma activation also impacts bone in humans. In addition, since type 2 diabetes is associated with higher fracture risk, an understanding of the clinical impact of TZDs on bone is needed to guide fracture prevention efforts in this population. This review summarizes current findings regarding type 2 diabetes and increased fracture risk and then considers the available evidence regarding TZD use and bone metabolism in humans.
啮齿动物和体外模型的证据表明，噻唑烷二酮（TZDs）激活过氧化物酶体增殖物激活受体-γ（PPAR-γ）会导致骨髓脂肪增多和成骨细胞生成减少，从而导致骨质流失。TZDs 被开处方用于治疗糖尿病，这为确定 PPAR-γ 激活是否也会影响人体骨骼提供了机会。此外，由于 2 型糖尿病与更高的骨折风险相关，因此需要了解 TZDs 对骨骼的临床影响，以指导该人群的骨折预防工作。这篇综述总结了目前关于 2 型糖尿病和骨折风险增加的研究结果，然后考虑了关于 TZD 应用和人类骨代谢的现有证据。
