Endocrine role of bone in the regulation of energy metabolism

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作者
Ruoyu Zhou
Qiaoyue Guo
Ye Xiao
Qi Guo
Yan Huang
Changjun Li
Xianghang Luo
机构
[1] Xiangya Hospital of Central South University,Department of Endocrinology, Endocrinology Research Center
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Bone Research | / 9卷
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摘要
Bone mainly functions as a supportive framework for the whole body and is the major regulator of calcium homeostasis and hematopoietic function. Recently, an increasing number of studies have characterized the significance of bone as an endocrine organ, suggesting that bone-derived factors regulate local bone metabolism and metabolic functions. In addition, these factors can regulate global energy homeostasis by altering insulin sensitivity, feeding behavior, and adipocyte commitment. These findings may provide a new pathological mechanism for related metabolic diseases or be used in the diagnosis, treatment, and prevention of metabolic diseases such as osteoporosis, obesity, and diabetes mellitus. In this review, we summarize the regulatory effect of bone and bone-derived factors on energy metabolism and discuss directions for future research.
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[31]  
Booth SL(2016)The PLC/PKC/Ras/MEK/Kv channel pathway is involved in uncarboxylated osteocalcin-regulated insulin secretion in rats Peptides 86 740-79
[32]  
Centi A(2018)Mechanisms of action and therapeutic application of glucagon-like peptide-1 Cell Metab. 27 68-1068
[33]  
Smith SR(2014)Oral administration of osteocalcin improves glucose utilization by stimulating glucagon-like peptide-1 secretion Bone 69 1055-1257
[34]  
Gundberg C(2013)Osteocalcin reverses endoplasmic reticulum stress and improves impaired insulin sensitivity secondary to diet-induced obesity through nuclear factor-κB signaling pathway Endocrinology 154 46-894.e13
[35]  
Hauschka PV(2017)Undercarboxylated osteocalcin reverts insulin resistance induced by endoplasmic reticulum stress in human umbilical vein endothelial cells Sci. Rep. 7 1250-433
[36]  
Lian JB(2013)The preventive effect of uncarboxylated osteocalcin against free fatty acid-induced endothelial apoptosis through the activation of phosphatidylinositol 3-kinase/Akt signaling pathway Metabolism 62 881-347
[37]  
Cole DE(2018)Quiescent endothelial cells upregulate fatty acid β-oxidation for vasculoprotection via redox homeostasis Cell Metab. 28 414-680
[38]  
Gundberg CM(2019)Hallmarks of endothelial cell metabolism in health and disease Cell Metab. 30 341-670
[39]  
Ducy P(2014)Carboxylated and uncarboxylated forms of osteocalcin directly modulate the glucose transport system and inflammation in adipocytes Horm. Metab. Res. 46 677-17
[40]  
Ishida M(2011)The osteoblast: an insulin target cell controlling glucose homeostasis J. Bone Min. Res. 26 664-9