1. Neuronal Induction of Bone-Fat Imbalance through Osteocyte Neuropeptide Y.
- Author
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Zhang Y, Chen CY, Liu YW, Rao SS, Tan YJ, Qian YX, Xia K, Huang J, Liu XX, Hong CG, Yin H, Cao J, Feng SK, He ZH, Li YY, Luo ZW, Wu B, Yan ZQ, Chen TH, Chen ML, Wang YY, Wang ZX, Liu ZZ, Luo MJ, Hu XK, Jin L, Wan TF, Yue T, Tang SY, and Xie H
- Subjects
- Adipogenesis physiology, Animals, Bone and Bones physiopathology, Disease Models, Animal, Female, Male, Mice, Mice, Inbred C57BL, Osteocytes metabolism, Osteogenesis physiology, Osteoporosis physiopathology, Adipocytes metabolism, Bone and Bones metabolism, Neuropeptide Y metabolism, Osteoblasts metabolism, Osteoporosis metabolism
- Abstract
A differentiation switch of bone marrow mesenchymal stem/stromal cells (BMSCs) from osteoblasts to adipocytes contributes to age- and menopause-associated bone loss and marrow adiposity. Here it is found that osteocytes, the most abundant bone cells, promote adipogenesis and inhibit osteogenesis of BMSCs by secreting neuropeptide Y (NPY), whose expression increases with aging and osteoporosis. Deletion of NPY in osteocytes generates a high bone mass phenotype, and attenuates aging- and ovariectomy (OVX)-induced bone-fat imbalance in mice. Osteocyte NPY production is under the control of autonomic nervous system (ANS) and osteocyte NPY deletion blocks the ANS-induced regulation of BMSC fate and bone-fat balance. γ-Oryzanol, a clinically used ANS regulator, significantly increases bone formation and reverses aging- and OVX-induced osteocyte NPY overproduction and marrow adiposity in control mice, but not in mice lacking osteocyte NPY. The study suggests a new mode of neuronal control of bone metabolism through the ANS-induced regulation of osteocyte NPY., (© 2021 The Authors. Advanced Science published by Wiley-VCH GmbH.)
- Published
- 2021
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