骨髓间质干细胞在糖尿病性骨质疏松发病中的作用

1型或2型糖尿病人患骨质疏松症和发生骨折的风险明显增加,其机制可能是由于骨髓间质干细胞(BMSCs)的耗竭。糖尿病通过高血糖等多种因素影响成骨细胞功能和骨形成,诱导骨髓细胞中脂肪累积,减少可用于骨形成的成骨细胞的数量,其中过氧化物酶体增殖物激活受体γ在BMSCs向成骨细胞或脂肪细胞分化上起着关键的闸门作用。由于糖尿病降低骨密度主要通过影响骨形成而非骨吸收,增加成骨细胞产生和禁止BMSCs流向脂肪细胞的途径,在理论上是预防和治疗糖尿病骨质疏松症的最根本方法。

Effects of Bone Marrow Mesenchymal Stem Cells on Diabetic Osteoporosis

The patients with type 1 or 2 diabetes mellitus have increased risk of osteoporosis and osteoporotic fractures significantly.The mechanism that induces diabetic osteoporosis may be due to the exhaust of bone marrow mesenchymal stem cells(BMSCs).It is apparent that hyperglycemia and varied factors in diabetes directly suppresses osteoblast-mediated bone formation and function,while conversely promoting adipogenic differentiation of BMSCs,and fat accumulation in the marrow cavity,all of which decrease the quantity of osteoblasts used for bone formation.Especially,the peroxisome proliferator-activated receptors γ is a gate-keeper for BMSCs differentiation into adipocytes and osteoblasts.Because diabetes mainly affects bone density by decreasing bone formation rather than increasing bone resorption,logically,it should be a most basic method to prevent and treat the diabetes induced osteoporosis by increasing osteoblasts and inhibiting the pathway of BMSCs differentiation toward adipocytes.