The role of vitamin d in the metabolic homeostasis of diabetic bone

Most studies across a variety of geographic locations suggest that vitamin D insufficiency is more common in individuals with type 1 diabetes (T1D) compared to the general population. In type 2 diabetes (T2D), while obesity is commonplace and lower vitamin D levels are present in obese adolescents and adults, the association between vitamin D insufficiency and T2D is less clear. Studies suggest that the relationship between T2D and vitamin D may be concurrently influenced by ethnicity, geography, BMI and age. Nonetheless, diabetic osteopathy is a significant comorbidity of both forms of diabetes and is characterized by micro-architectural changes that decrease bone quality leading to an increased risk for bone fracture in both disorders. The question remains, however, to what degree vitamin D homeostasis contributes to or exacerbates skeletal pathology in diabetes. Proposed mechanisms for vitamin D deficiency in diabetes include (1) genetic predisposition (T1D); (2) increased BMI (T2D); (3) concurrent albuminuria (T1D or T2D); or (4) exaggerated renal excretion of vitamin D metabolites or vitamin D-binding protein (T1D, T2D, animal models). The specific effects of vitamin D treatment on diabetic osteoporosis have been examined in rodents and demonstrate skeletal improvements even in the face of untreated diabetes. However, human clinical trial data examining whether vitamin D status can be directly related to or it is predictive of bone quality and fracture risk in those with diabetes are still needed. Herein, we provide a review of the literature linking vitamin D, diabetes and skeletal health.