On the regulation of bone metabolism: A research review of neuropeptide Y
10.3760/cma.j.issn.1000-6699.2018.11.017
- VernacularTitle:神经肽Y与骨代谢研究进展
- Author:
Kaiqiang SUN
1
;
Le HUAN
;
Ximing XU
;
Jiangang SHI
Author Information
1. 第二军医大学长征医院第二脊柱外科
- Keywords:
Neuropeptide Y;
Bone metabolism;
Osteoporosis;
Fracture;
Glucose homeostasis;
Fat metabolism;
Energy metabolism;
Treatment
- From:
Chinese Journal of Endocrinology and Metabolism
2018;34(11):982-986
- CountryChina
- Language:Chinese
-
Abstract:
Skeleton metabolic diseases such as osteoporosis and fracture have posed an detrimental impact on the elderly, which is a primary cause of paralysis and even death in patients. Osteoblast and osteoclast are the two major parts in the regulation of bone homeostasis and imbalance of these two cells, which may result in dysfunction of bone metabolism. Recent researches indicated that bone homeostasis was primarily regulated by endocrine, paracrine, and local mechanical processes. However, increasing evidences have indicated that the significant role of nerve system may involve in bone metabolism via both central and peripheral pathways. Neuropeptide Y(NPY), a neurotransmitter that belongs to a family of peptides,serves as a critical hinge connecting nerve system and skeleton system. Several studies have suggested that NPY generated by both central and peripheral nerve system could regulate bone homeostasis and that NPY-energic nerve fibers distributed on bone surface and in intramedullary cavity and NPY receptors located at osteoblast, chondrocyte, and osteocytes also provide a basis for nerve-skeleton metabolic pathways. NPY can directly regulate osteoprogenitor, involving in the production and differentiation of osteoblast and osteoclast. In addition, as a pivotal molecular of energy homeostasis, NPY may affect glucose and fat homeostasis. Studies of animal models also have further indicated energy metabolism may directly or indirectly participate in the regulation of bone mass. Therefore, further researches on the relationship between NPY and bone homeostasis may facilitate to unveil the central and peripheral regulatory effect of NPY on bone homeostasis and provide a new sight for the treatment of skeleton metabolism-related diseases in the future.
