Influence of diabetic state and vitamin D deficiency on bone repair in female mice

- Vitamin D (VD) deficiency does not affect bone repair in normal and diabetic mice.
- VD deficiency augments diabetic bone loss in mice.
- Diabetic state blunts the levels of osteogenic genes enhanced by VD deficiency.

Type 1 diabetes is associated with an increased fracture risk, an impaired fracture healing, and an increased vitamin D insufficiency. However, the role of vitamin D in diabetic bone repair process remains unclear. We therefore examined the effects of vitamin D deficiency on the impaired bone repair in streptozotocin (STZ)-induced diabetes using female mice. Diabetes was induced by STZ injection into female mice after feeding with normal or vitamin D-deficient diet for 6 weeks from the age of 4 weeks. A femoral bone defect was induced in mice 4 weeks after induction of diabetes. The repair of damaged site on the femur was significantly delayed at days 7 and 10 after bone defect by diabetic state in mice, as assessed by quantitative computed tomography, while vitamin D deficiency did not affect the bone repair both in mice with normal and diabetic state. The decreases in bone mineral density (BMD) at cortical and trabecular bone by diabetic state were significantly augmented by vitamin D deficiency in tibia at the undamaged side in mice. Diabetic state blunted the levels of osteogenic and chondrogenic genes enhanced by vitamin D deficiency. Moreover, vitamin D deficiency significantly aggravated the decreases in osteocalcin and IGF-1 mRNA by diabetic state. In conclusion, our study showed that vitamin D deficiency aggravates the decrease in BMD by diabetic state in female mice, although vitamin D deficiency did not affect bone repair delayed by diabetic state.