Hayakawa Nobuki, Suzuki Atsushi
Clinical Pharmacotherapeutics I, Faculty of Pharmacy, Meijo University, Nagoya, Aichi, Japan.
Clin Calcium. 2012 Sep;22(9):1383-90.
Type 2 diabetes is closely associated with fragility fracture risk. Metabolic control of diabetes may improve bone status, but several anti-diabetic medicines could directly affect bone metabolism. Thiazolidinediones (TZD) may have a negative effect by switching mesenchymal progenitor cells to adipose rather than bone tissue. Clinical trials and meta-analyses showed that elderly women taking TZD could be at increased risk of fractures. On the contrary, in vitro studies suggest that incretin mimetics and incretin enhancers could positively regulate bone metabolism. Dipeptidyl peptidase-4 (DPP-4) inhibitors, which enhance serum incretin concentration, have been reported to reduce clinical fractures. However, further studies would be required for their long term-efficacy and safety on bone metabolism.
2型糖尿病与脆性骨折风险密切相关。糖尿病的代谢控制可能会改善骨状态,但几种抗糖尿病药物可能会直接影响骨代谢。噻唑烷二酮类药物(TZD)可能会通过将间充质祖细胞转变为脂肪组织而非骨组织而产生负面影响。临床试验和荟萃分析表明,服用TZD的老年女性骨折风险可能会增加。相反,体外研究表明,肠促胰岛素类似物和肠促胰岛素增强剂可以正向调节骨代谢。据报道,可提高血清肠促胰岛素浓度的二肽基肽酶-4(DPP-4)抑制剂可减少临床骨折。然而,它们对骨代谢的长期疗效和安全性还需要进一步研究。