Considering that the potential osteoprotective property of BNP reported by some studies [7, 9, 13–17] and the cumulative effects of natriuretic peptides oppose the physiologic abnormalities of HF, instead of begetting HF [7], there is a possibility that circulating BNP may be upregulated to compensate for lower BMD and increased risk of osteoporosis in response to cardio-metabolic risk factors, inflammation orvascular damage in T2DM patients, and circulating BNP might be a potential biomarker for osteoporosis in patients with T2DM. This evidence concerns the gene NPPB and hydrops fetalis.