Osteoporosis affects 200 million people worldwide. Osteoporosis in subjects with diabetes is called diabetoporosis, and type 2 diabetes (T2D) contributes to and aggravates osteoporotic fractures. Hyperglycemia, insulin resistance, bone vasculature impairment, increased inflammation, oxidative stress, and bone marrow adiposity contribute to a higher incidence of osteoporotic fractures in T2D. Decreased nitric oxide (NO) bioavailability due to lower endothelial NO synthase (eNOS)-derived NO and higher inducible NOS (iNOS)-derived NO is one of the main mechanisms of the diabetoporosis. Available data indicates that T2D increases osteoclast-mediated bone resorption and decreases osteoblast-mediated bone formation, mediated in part by reducing eNOS-derived NO and increasing iNOS-derived NO. NO donors delay osteoporosis and decrease osteoporotic fractures in subjects with T2D, suggesting the potential therapeutic implication of NO-based interventions for diabetoporosis.
Keywords: Bone mineral density, Bone marrow stromal cells, Diabetoporosis, Endothelial nitric oxide synthase, Inducible nitric oxide synthase, Nitric oxide, Osteoporosis, Type 2 diabetes.
