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Energy Metabolism of Bone

Overview
Journal Toxicol Pathol
Publisher Sage Publications
Date 2017 Nov 4
PMID 29096593
Citations 25
Authors
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Abstract

Biological processes utilize energy and therefore must be prioritized based on fuel availability. Bone is no exception to this, and the benefit of remodeling when necessary outweighs the energy costs. Bone remodeling is important for maintaining blood calcium homeostasis, repairing micro cracks and fractures, and modifying bone structure so that it is better suited to withstand loading demands. Osteoclasts, osteoblasts, and osteocytes are the primary cells responsible for bone remodeling, although bone marrow adipocytes and other cells may also play an indirect role. There is a renewed interest in bone cell energetics because of the potential for these processes to be targeted for osteoporosis therapies. In contrast, due to the intimate link between bone and energy homeostasis, pharmaceuticals that treat metabolic disease or have metabolic side effects often have deleterious bone consequences. In this brief review, we will introduce osteoporosis, discuss how bone cells utilize energy to function, evidence for bone regulating whole body energy homeostasis, and some of the unanswered questions and opportunities for further research in the field.

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References
1.
Slade J, Coe L, Meyer R, McCabe L . Human bone marrow adiposity is linked with serum lipid levels not T1-diabetes. J Diabetes Complications. 2012; 26(1):1-9. DOI: 10.1016/j.jdiacomp.2011.11.001. View

2.
Burge R, Dawson-Hughes B, Solomon D, Wong J, King A, Tosteson A . Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2006; 22(3):465-75. DOI: 10.1359/jbmr.061113. View

3.
Diaz-Ruiz R, Rigoulet M, Devin A . The Warburg and Crabtree effects: On the origin of cancer cell energy metabolism and of yeast glucose repression. Biochim Biophys Acta. 2010; 1807(6):568-76. DOI: 10.1016/j.bbabio.2010.08.010. View

4.
Mills K, Yoshida S, Stein L, Grozio A, Kubota S, Sasaki Y . Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2017; 24(6):795-806. PMC: 5668137. DOI: 10.1016/j.cmet.2016.09.013. View

5.
McCabe L . Understanding the pathology and mechanisms of type I diabetic bone loss. J Cell Biochem. 2007; 102(6):1343-57. DOI: 10.1002/jcb.21573. View