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Osteocalcin promotes bone mineralization but is not a hormone


Autoři: Stavros C. Manolagas aff001
Působiště autorů: Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Arkansas, United States of America aff001;  Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, United States of America aff002
Vyšlo v časopise: Osteocalcin promotes bone mineralization but is not a hormone. PLoS Genet 16(6): e1008714. doi:10.1371/journal.pgen.1008714
Kategorie: Perspective
doi: https://doi.org/10.1371/journal.pgen.1008714


Zdroje

1. Manolagas SC. (2000) Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr Rev. 21:115–37. doi: 10.1210/edrv.21.2.0395 10782361

2. Ducy P, Desbois C, Boyce B, Pinero G, Story B, et al. (1996) Increased bone formation in osteocalcin-deficient mice. Nature. 1:448–52.

3. Lee NK, Sowa H, Hinoi E, Ferron M, Ahn JD, et al. (2007) Endocrine regulation of energy metabolism by the skeleton. Cell 130:456–469. doi: 10.1016/j.cell.2007.05.047 17693256

4. Oury F, Sumara G, Sumara O, Ferron M, Chang H, et al. (2011) Endocrine regulation of male fertility by the skeleton. Cell. 144:796–809. doi: 10.1016/j.cell.2011.02.004 21333348

5. Oury F, Khrimian L, Denny CA, Gardin A, Chamouni A, et al. (2013) Maternal and offspring pools of osteocalcin influence brain development and functions. Cell. 26:228–41.

6. Mera P, Laue K, Wei J, Berger JM, Karsenty G. (2016) Osteocalcin is necessary and sufficient to maintain muscle mass in older mice. Mol Metab. 16:1042–1047.

7. Karsenty G. (2017) Update on the biology of osteocalcin. Endocr Pract. 23:1270–1274. doi: 10.4158/EP171966.RA 28704102

8. Ferron M and Karsenty G. Regulation of energy metabolism by bone-derived hormones. In Principles of Bone Biology. Bilezikian JP, Martin TJ, Clemens TL, Rosen CJ (eds). Academic Press 2020.

9. Wellendorph P, Johansen LD, Jensen AA, Casanova E, Gassmann M, et al. No evidence for a bone phenotype in GPRC6A knockout mice under normal physiological conditions. (2009) J Mol Endocrinol. 42: 215–223. doi: 10.1677/JME-08-0149 19103720

10. Jørgensen CV, Gasparini SJ, Tu J, Zhou H, Seibel MJ, et al. (2019) Metabolic and skeletal homeostasis are maintained in full locus GPRC6A knockout mice. Scientific reports. 9:5995 doi: 10.1038/s41598-019-41921-8 30979912

11. Smajilovic S, Clemmensen C, Johansen LD, Wellendorph P, Holst JJ, et al. (2013) The L-alpha-amino acid receptor GPRC6A is expressed in the islets of Langerhans but is not involved in L-arginine-induced insulin release. Amino acids. 44:383–390. doi: 10.1007/s00726-012-1341-8 22714012

12. Lambert LJ, Challa AK, Niu A, Zhou L, Tucholski J, et al. (2016) Increased trabecular bone and improved biomechanics in an osteocalcin-null rat model created by CRISPR/Cas9 technology. Dis Model Mech. 9:1169–1179. doi: 10.1242/dmm.025247 27483347

13. Moriishi T, Ozasa R, Ishimoto T, Nakano T, Hasegawa T, et al. (2020) Osteocalcin is necessary for the alignment of apatite crystallites, but not glucose metabolism, testosterone synthesis, or muscle mass. PLoS Genetics. 16:e1008586. https://doi.org/10.1371/journal.pgen.1008586

14. Diegel CR, Hann S, Ayturk U, Hu JCW, Lim K, et al. (2020) An osteocalcin-deficient mouse strain without endocrine abnormalities. PLoS Genetics. 16:e1008361. https://doi.org/10.1371/journal.pgen.1008361

15. National Academies of Sciences, Engineering, and Medicine, Policy and Global Affairs, Committee on Science, Engineering, Medicine, and Public Policy, Committee on Responsible Science (2017) Fostering Integrity in Research. Washington (DC): National Academies Press (US); Apr 11. doi: 10.17226/21896 29341557.

16. Manolagas SC, Kronenberg HM. (2014) Reproducibility of results in preclinical studies: a perspective from the bone field. J Bone Miner Res. 29:2131–40. doi: 10.1002/jbmr.2293 24916175


Článek vyšel v časopise

PLOS Genetics


2020 Číslo 6
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