Some studies have reported associations between cardiovascular diseases (CVD) and bone mineral loss. Osteoclast regulatory factors can affect vascular calcifications, and a high blood pressure can induce abnormalities in calcium metabolism and increase bone mineral loss in women. Low bone mineral density is not only an important predictor of osteoporotic fracture, but is also a risk factor for mortality.
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The osteoblast-specific secreted molecule osteocalcin behaves as a hormone regulating glucose metabolism and fat mass in two mutant mouse strains [1]. In a recent study [2], the authors asked two questions: is the action of osteocalcin on β-cells and adipocytes elicited by the same concentrations of the molecule, and more importantly, does osteocalcin regulate energy metabolism in wild-type mice? Cell-based assays using isolated pancreatic islets, a β-cell line, and primary adipocytes showed that picomolar amounts of osteocalcin are sufficient to regulate the expression of the insulin genes and β-celll proliferation markers, whereas nanomolar amounts affect adiponectin and Pgc1α expression in white and brown adipocytes, respectively.
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