1,25(OH)₂D₃ inhibits the deleterious effects induced by high glucose on osteoblasts through undercarboxylated osteocalcin and insulin signaling
2012
Wu, Ying Ying | Yu, Tao | Zhang, Xiao-hui | Liu, Yan-shan | Li, Feng | Wang, Yan-ying | Wang, Yong-yue | Gong, Ping
Diabetes mellitus (DM) is associated with multiple skeletal disorders, and vitamin D may play a functional role in the preservation of glucose tolerance. However, the relationship between vitamin D deficiency and DM is not well known. The aim of this study was to investigate the potential molecular link between 1,25(OH)₂D₃ regulation and glucose homeostasis. Rat primary osteoblasts were cultured in different conditioned medium: normal glucose, high glucose, high glucose and insulin, high glucose and 1,25(OH)₂D₃, high glucose and insulin and 1,25(OH)₂D₃. The activity of osteoblasts was measured by cell viability, alkaline phosphatase and osteocalcin assay. The potential mechanism of how 1,25(OH)₂D₃ affect insulin sensitivity was investigated by the assay of insulin receptor (IR) and vitamin D receptor (VDR) expression, and undercarboxylated osteocalcin (ucOC) level. The combined treatment has the strongest effect of inhibiting the deleterious effects induced by high glucose on osteoblasts, and it promoted the %ucOC value to approximately 40%, which is much higher than that in high glucose without treatment. Levels of IR and VDR of osteoblasts in combined treatment culture increased significantly compared with that in high glucose without treatment. So maybe 1,25(OH)₂D₃ promotes insulin sensitivity of osteoblasts by activating insulin signaling and simultaneously stimulating ucOC secretion, which in turn regulate insulin production and sensitivity. 1,25(OH)₂D₃ might be beneficial not only for diabetes, but also, for osteoporosis by promoting bone formation.
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