Abstract
Accumulating evidence indicates close and tight relationship between bone tissue and energy expenditure, especially glucose metabolism. In molecular mechanisms, osteocalcin secreted from osteoblasts, as a hormone, is demonstrated in mice to be involved not only in insulin secretion from islet β-cells but also in insulin resistance in adipose tissue. In addition, since signaling cascades in liver activated by RANK ligand has been shown to participate in augmentation of insulin resistance, pharmacological inhibition of RANK ligand for treatment of osteoporosis is speculated to improve insulin resistance in human. However, data from several clinical trials of ant-osteoporosis drugs have not supported an idea that they were clinically involved in glucose metabolism. Interestingly, some retrospective observational studies demonstrate that long-term administration of bisphosphonates may decrease the incidence of newly onset of type 2 diabetes, although mechanisms by which they do so are totally uncertain.
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