Diabetes mellitus is a prevalent disease result in several complications, including bone problems. Previous studies have shown that microRNA (miR)-26a regulates glucose metabolism and plays a protective role in diabetes. However, whether miR-26a also affects bone quality in diabetes remains unknown. In the present study, we evaluated the potential effects of miR-26a on bone in diabetic mice. We administrated miR-26a in streptozotocin-induced diabetic mice. The metabolic parameters, bone quality, osteoblast and osteoclast markers, and insulin signaling activation were measured. miR-26a ameliorated insulin resistance and glucose tolerance, improved bone microarchitecture and quality, increased osteoblasts and bone formation, decreased osteoclasts, and promoted the insulin signaling pathway in diabetic mice. These effects were abolished in insulin receptor-compromised Col1a1-Insr^+/– mice. In conclusion, miR-26a could ameliorate bone-specific insulin resistance and bone quality in diabetic mice, which depended on the insulin receptors on osteoblasts. Our findings highlight the potential of miR-26a as a therapeutic target for diabetes mellitus-related bone metabolism and diseases.

糖尿病是导致多种并发症（包括骨骼问题）的普遍疾病。先前的研究表明，microRNA（miR）-26a调节葡萄糖代谢并在糖尿病中起保护作用。然而，miR-26a是否也影响糖尿病的骨质量仍然未知。在本研究中，我们评估了miR-26a对糖尿病小鼠骨骼的潜在影响。我们在链脲佐菌素诱导的糖尿病小鼠中施用miR-26a。测量了代谢参数，骨质量，成骨细胞和破骨细胞标志物以及胰岛素信号激活。miR-26a改善了胰岛素抵抗和葡萄糖耐量，改善了骨微结构和质量，增加了成骨细胞和骨形成，减少了破骨细胞，并促进了糖尿病小鼠的胰岛素信号通路。^+/–小鼠。总之，miR-26a可以改善糖尿病小鼠的骨特异性胰岛素抵抗和骨骼质量，这取决于成骨细胞上的胰岛素受体。我们的发现强调了miR-26a作为糖尿病相关骨代谢和疾病的治疗靶标的潜力。