My research interest is to elucidate the molecular mechanism of bone and cartilage metabolism by means of genetics and physiology. Skeleton is an organ mainly composed of three distinct sets of cell types: chondrocytes, osteoblasts, and osteoclasts. Deterioration of any of these cell populations leads to the destruction of normal bone development or mineral homeostasis. Therefore, studying the biology of these cells is extremely important for the cure of bone and cartilage degenerative diseases.
We demonstrated that leptin regulates bone metabolism by modulating sympathetic nervous system activity through the hypothalamus and blockade of sympathetic nervous system activity by beta-blockers ameliorates bone loss in mice and others. This regulatory mechanism through which the central nervous system controls bone has now been demonstrated to be true in humans by many subsequent clinical studies. These studies opened a new field of bone biology, giving rise to new chapters on the “central control of bone metabolism” in many textbooks. Then, we demonstrated that neuromedin U, an anorexigenic neuropeptide, regulates bone remodeling through the central nervous system by affecting the expression of molecular clock proteins in osteoblasts, independent of any known neuronal pathways regulating bone metabolism. This work confirms the importance of central control of bone remodeling. Recently, we demonstrated that vitamin E (α-tocopherol) increases bone resorption by stimulating osteoclast fusion and that wild-type mice or rats fed a α-tocopherol–supplemented diet lost bone. This study suggests that vitamin E may cause bone loss in humans.