Osteoporosis is a systemic skeletal disorder that remains a major public health problem due to significant fracture-associated morbidity and mortality. Because it has been shown that individuals having type I diabetes mellitus also suffer from osteopenia or osteoporosis, there is probably a pathophysiological mechanism that links pancreatic beta cell insufficiency with inappropriate bone formation. Many factors have been suggested, including amylin, a product of pancreatic beta cells with structural and functional similarity to calcitonin. Amylin has been shown to stimulate bone development via action on osteoblasts and osteoclasts. Recently, amylin receptors have been identified as complexed calcitonin receptor with receptor activity modifying proteins. Moreover, a synthetic amylin analogue (pramlintide) has been developed for clinical use. These findings including results from in vitro animal and human studies suggest a role for amylin as a potential diagnostic and therapeutical tool in patients with various bone diseases including osteoporosis. However, other structurally and functionally related hormones that affect bone metabolism should also be taken in account including calcitonin, calcitonin gene-related peptide and adrenomedullin.