Abstract
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.
Highlights
Diabetes mellitus (DM), which is commonly known as diabetes, is a metabolic disease characterized by high blood sugar.[1]
High serum glucose concentrations inhibit the production of bone-formation marker osteocalcin (OCN), which impaired bone formation.[3]
We demonstrated that miR-26a ameliorated glucose and insulin levels and improved bone microarchitecture and bone thickness in diabetic mice. miR-26a promoted osteoblasts and bone formation, whereas it prevented osteoclast differentiation
Summary
Diabetes mellitus (DM), which is commonly known as diabetes, is a metabolic disease characterized by high blood sugar.[1]. Diabetes is a major cause of cardiovascular disease, kidney failure, neuropathy, and blindness, which are significant causes of morbidity and mortality in diabetic patients.[2] insulin-like growth factor 1 (IGF-1) and transforming growth factor b1 (TGF-b1), are differentially expressed, which contributes to decreased bone growth.[6]. The miR-26 family, which is composed of miR-26a and miR-26b, plays a crucial role in tumorigenesis by targeting critical regulators involved in development, cell cycle, and differentiation. MiR-26a acts as a potent tumor suppressor in the liver, the central organ involved in maintaining glucose and lipid homeostasis.[7] miR-26a-overexpressing/transgenic mice have improved insulin sensitivity, decreased glucose level, and decreased fatty acid synthesis. Inhibition of miR-26a results in impaired insulin sensitivity and increased glucose level.[7]
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