Patients with diabetes have been widely reported to be at an increased risk of secondary osteoporosis. Osteoporosis is caused by an imbalance in bone remodeling due to increased bone resorption and/or decreased osteoblast-dependent bone formation. In this study, mesenchymal stem cells (MSCs) were used as a disease model to determine the effects of high glucose levels on MSC-osteoblast development. The results indicated that under high glucose conditions, MSCs had reduced cell viability and increased number of β-galactosidase-positive cells. Furthermore, in vitro osteogenesis was shown to be reduced in MSCs cultured in osteogenic differentiation medium at 10, 25, and 40 mM glucose as demonstrated by Alizarin red S staining and alkaline phosphatase activity assay. Moreover, a proteomic study was performed in MSCs cultured with 25 and 40 mM glucose. The proteomic results demonstrated that 12 proteins were up- and downregulated in bone marrow-derived mesenchymal stem cells cultured with high glucose in a dose-dependent manner. The findings presented here contribute to our understanding of the mechanism of diabetes mellitus responsible for bone loss. However, the exact mechanism of action of hyperglycemia on bone deformability requires additional studies.

广泛报道糖尿病患者继发性骨质疏松症的风险增加。骨质疏松症是由于骨吸收增加和/或成骨细胞依赖性骨形成减少而导致的骨骼重塑失衡引起的。在这项研究中，间充质干细胞（MSCs）被用作疾病模型，以确定高葡萄糖水平对MSC成骨细胞发育的影响。结果表明，在高葡萄糖条件下，间充质干细胞活力降低，β-半乳糖苷酶阳性细胞数量增加。此外，通过茜素红S染色和碱性磷酸酶活性测定法证实，在成骨分化培养基中以10、25和40 mM葡萄糖培养的MSC中，体外成骨作用降低。此外，在用25和40 mM葡萄糖培养的MSC中进行了蛋白质组学研究。蛋白质组学结果表明，在高糖培养的骨髓来源的间充质干细胞中，有12种蛋白被上调和下调，呈剂量依赖性。此处提出的发现有助于我们理解造成骨质流失的糖尿病机制。但是，高血糖对骨骼变形的确切作用机理尚需进一步研究。