Neuronal Induction of Bone‐Fat Imbalance through Osteocyte Neuropeptide Y

• DOI: 10.1002/advs.202100808
• Publication Date: 2021-11-01T06:56:53Z
• Authors: Yan Zhang; Chun‐Yuan Chen; Yi‐Wei Liu; Shan‐Shan Rao; Yi‐Juan Tan; Yu‐Xuan Qian; Kun Xia; Jie Huang; Xi‐Xi Liu; Chun‐Gu Hong; Hao Yin; Jia Cao; Shi‐Kai Feng; Ze‐Hui He; You‐You Li; Zhong‐Wei Luo; Ben Wu; Zi‐Qi Yan; Tuan‐Hui Chen; Meng‐Lu Chen; Yi‐Yi Wang; Zhen‐Xing Wang; Zheng‐Zhao Liu; Ming‐Jie Luo; Xiong‐Ke Hu; Ling Jin; Teng‐Fei Wan; Tao Yue; Si‐Yuan Tang; Hui Xie
• Keywords: Osteocyte; Bone remodeling

Abstract A differentiation switch of bone marrow mesenchymal stem/stromal cells (BMSCs) from osteoblasts to adipocytes contributes age‐ and menopause‐associated loss adiposity. Here it is found that osteocytes, the most abundant cells, promote adipogenesis inhibit osteogenesis BMSCs by secreting neuropeptide Y (NPY), whose expression increases with aging osteoporosis. Deletion NPY in osteocytes generates a high mass phenotype, attenuates aging‐ ovariectomy (OVX)‐induced bone‐fat imbalance mice. Osteocyte production under control autonomic nervous system (ANS) osteocyte deletion blocks ANS‐induced regulation BMSC fate balance. γ ‐Oryzanol, clinically used ANS regulator, significantly formation reverses OVX‐induced overproduction adiposity mice, but not mice lacking NPY. The study suggests new mode neuronal metabolism through