Bone adjusts its structure to become better suited to withstand the mechanical demands it experiences. Physical loading and routine activities have been shown to inhibit bone resorption. However, the cellular mechanism underlying this phenomenon remains largely unknown. The focus of a recent study [1] was to determine the mechanisms by which osteocytes might transduce and regulate bone resorption, and the antiresorptive effects of loading.
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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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The differentiation of multipotent stemcells of mesodermal origin results in the formation of adipocytes, chondrocytes, osteoblasts, and myoblasts. In humans, osteoporosis and age-related osteopenia are associated with an increase in marrow fat tissue and osteoblast numbers correlated negatively with the number of adipocytes. Osteoblastic differentiation is driven by runx2, and then characterized by the expression of alkaline phosphatase, osteocalcin, and eventually by the mineralization of the extracellular matrix.
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