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本文引用的文献

1
Mechanism of Bone Mineralization.骨矿化机制。
Cold Spring Harb Perspect Med. 2018 Dec 3;8(12):a031229. doi: 10.1101/cshperspect.a031229.
2
Neural Regulation of Bone and Bone Marrow.神经调节骨骼和骨髓。
Cold Spring Harb Perspect Med. 2018 Sep 4;8(9):a031344. doi: 10.1101/cshperspect.a031344.
3
Regulation of Bone Remodeling by Parathyroid Hormone.甲状旁腺激素对骨重塑的调节。
Cold Spring Harb Perspect Med. 2018 Aug 1;8(8):a031237. doi: 10.1101/cshperspect.a031237.
4
Multiple Myeloma and Bone: The Fatal Interaction.多发性骨髓瘤与骨骼:致命交互。
Cold Spring Harb Perspect Med. 2018 Aug 1;8(8):a031286. doi: 10.1101/cshperspect.a031286.
5
The Bone Marrow Microenvironment in Health and Myeloid Malignancy.骨髓微环境与髓系恶性肿瘤。
Cold Spring Harb Perspect Med. 2018 Jul 2;8(7):a031328. doi: 10.1101/cshperspect.a031328.
6
Regulation of Bone Metabolism by Sex Steroids.性激素对骨代谢的调节。
Cold Spring Harb Perspect Med. 2018 Jan 2;8(1):a031211. doi: 10.1101/cshperspect.a031211.
7
MC4R-dependent suppression of appetite by bone-derived lipocalin 2.骨源视黄醇结合蛋白2通过MC4R抑制食欲
Nature. 2017 Mar 16;543(7645):385-390. doi: 10.1038/nature21697. Epub 2017 Mar 8.
8
Association between osteocalcin gamma-carboxylation and insulin resistance in overweight and obese postmenopausal women.超重和肥胖绝经后女性骨钙素γ-羧化与胰岛素抵抗之间的关联
J Diabetes Complications. 2017 Jun;31(6):1027-1034. doi: 10.1016/j.jdiacomp.2017.01.023. Epub 2017 Feb 13.
9
Wnt/β-catenin signaling in osteoblasts regulates global energy metabolism.成骨细胞中的Wnt/β-连环蛋白信号传导调节整体能量代谢。
Bone. 2017 Apr;97:175-183. doi: 10.1016/j.bone.2017.01.028. Epub 2017 Jan 23.
10
Osteocalcin Improves Metabolic Profiles, Body Composition and Arterial Stiffening in an Induced Diabetic Rat Model.骨钙素改善诱导型糖尿病大鼠模型的代谢指标、身体组成和动脉僵硬度。
Exp Clin Endocrinol Diabetes. 2017 Apr;125(4):234-240. doi: 10.1055/s-0042-122138. Epub 2017 Jan 10.

骨源激素对能量代谢的调节。

Regulation of Energy Metabolism by Bone-Derived Hormones.

机构信息

Columbia University Medical Center, New York, New York 10032.

Institut de Recherches Cliniques de Montréal, Montréal, Quebec H2W 1R7, Canada.

出版信息

Cold Spring Harb Perspect Med. 2018 Jun 1;8(6):a031666. doi: 10.1101/cshperspect.a031666.

DOI:10.1101/cshperspect.a031666
PMID:28778968
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5983159/
Abstract

Like many other organs, bone can act as an endocrine organ through the secretion of bone-specific hormones or "osteokines." At least two osteokines are implicated in the control of glucose and energy metabolism: osteocalcin (OCN) and lipocalin-2 (LCN2). OCN stimulates the production and secretion of insulin by the pancreatic β-cells, but also favors adaptation to exercise by stimulating glucose and fatty acid (FA) utilization by the muscle. Both of these OCN functions are mediated by the G-protein-coupled receptor GPRC6A. In contrast, LCN2 influences energy metabolism by activating appetite-suppressing signaling in the brain. This action of LCN2 occurs through its binding to the melanocortin 4 receptor (MC4R) in the paraventricular nucleus of the hypothalamus (PVN) and ventromedial neurons of the hypothalamus.

摘要

与许多其他器官一样,骨骼可以通过分泌特定于骨骼的激素或“骨因子”来充当内分泌器官。至少有两种骨因子参与了葡萄糖和能量代谢的控制:骨钙素(OCN)和脂钙素 2(LCN2)。OCN 刺激胰岛 β 细胞产生和分泌胰岛素,但也通过刺激肌肉利用葡萄糖和脂肪酸(FA)来促进对运动的适应。OCN 的这两种功能均由 G 蛋白偶联受体 GPRC6A 介导。相比之下,LCN2 通过激活下丘脑室旁核(PVN)和下丘脑腹内侧神经元中的食欲抑制信号来影响能量代谢。LCN2 的这种作用是通过其与下丘脑室旁核和下丘脑腹内侧神经元中的黑皮质素 4 受体(MC4R)结合来实现的。