These data together would indicate the possibility that ischemia and hypoxia due to diabetic vascular diseases can lead to BNP production via wall motion abnormalities and increased wall stress or that ischemia can directly promote BNP to release, independent of cardiomyocytes [39, 40], and compensatory increase in circulating BNP in patients with diabetic osteoporosis may exert osteoprotective effect by promoting vessel creation, regulating vascular inflammation, improving endothelial function, atherosclerosis and blood supply to the bones [38]. The gene discussed is NPPB; the disease is atherosclerosis.