Institut de Recherches Cliniques de Montréal, Montréal, Québec, Canada H2W 1R7.
Mol Metab. 2013 Aug 15;2(4):498-504. doi: 10.1016/j.molmet.2013.08.004. eCollection 2013.
Osteocalcin is a hormone produced in bones by osteoblasts and regulating energy metabolism. While osteocalcin exists in two forms, γ-carboxylated and undercarboxylated only the latter appears to function as a hormone in vivo. It has been proposed recently that osteoclasts, the bone-resorbing cells, are responsible of decarboxylating, i.e. activating osteocalcin. To address the role of osteoclasts in the maintenance of energy metabolism we analyzed mutant mouse strains harboring either an increase or a decrease in osteoclasts number. Osteoprotegerin-deficient mice that are characterized by an increase in the number of osteoclasts demonstrate an increase in serum levels of undercarboxylated osteocalcin and are significantly more glucose tolerant than WT animals. Conversely, osteoclasts ablation in mice results in a decrease in serum undercarboxylated osteocalcin levels and in reduced glucose tolerance. These results support the notion that osteoclasts are controlling glucose metabolism at least in part through the regulation of osteocalcin decarboxylation.
骨钙素是成骨细胞产生的一种激素，调节能量代谢。骨钙素存在两种形式，γ-羧化和非羧化，只有后者似乎在体内发挥激素功能。最近有人提出，破骨细胞（骨吸收细胞）负责脱羧化，即激活骨钙素。为了研究破骨细胞在维持能量代谢中的作用，我们分析了破骨细胞数量增加或减少的突变小鼠品系。破骨细胞生成素缺陷小鼠的破骨细胞数量增加，其血清中非羧化骨钙素水平升高，对葡萄糖的耐受性明显高于 WT 动物。相反，在小鼠中消融破骨细胞会导致血清中非羧化骨钙素水平降低和葡萄糖耐量降低。这些结果支持这样一种观点，即破骨细胞至少部分通过调节骨钙素脱羧化来控制葡萄糖代谢。
