Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10720
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dc.contributor.authorChiang, Cherie Yingen
dc.contributor.authorChiu, Mariaen
dc.contributor.authorMoore, Alison Jen
dc.contributor.authorAnderson, Paul Hen
dc.contributor.authorGhasem-Zadeh, Alien
dc.contributor.authorMcManus, Julie Fen
dc.contributor.authorMa, Cathyen
dc.contributor.authorSeeman, Egoen
dc.contributor.authorClemens, Thomas Len
dc.contributor.authorMorris, Howard Aen
dc.contributor.authorZajac, Jeffrey Den
dc.contributor.authorDavey, Rachel Aen
dc.date.accessioned2015-05-16T00:15:40Z
dc.date.available2015-05-16T00:15:40Z
dc.date.issued2009-04-01en
dc.identifier.citationJournal of Bone and Mineral Research : the Official Journal of the American Society For Bone and Mineral Research; 24(4): 621-31en
dc.identifier.govdoc19049333en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10720en
dc.description.abstractAndrogens play a key role in skeletal growth and bone maintenance; however, their mechanism of action remains unclear. To address this, we selectively deleted the androgen receptor (AR) in terminally differentiated, mineralizing osteoblasts using the Cre/loxP system in mice (osteocalcin-Cre AR knockouts [mOBL-ARKOs]). Male mOBL-ARKOs had decreased femoral trabecular bone volume compared with littermate controls because of a reduction in trabecular number at 6, 12, and 24 wk of age, indicative of increased bone resorption. The effects of AR inactivation in mineralizing osteoblasts was most marked in the young mutant mice at 6 wk of age when rates of bone turnover are high, with a 35% reduction in trabecular bone volume, decreased cortical thickness, and abnormalities in the mineralization of bone matrix, characterized by increased unmineralized bone matrix and a decrease in the amount of mineralizing surface. This impairment in bone architecture in the mOBL-ARKOs persisted throughout adulthood despite an unexpected compensatory increase in osteoblast activity. Our findings show that androgens act through the AR in mineralizing osteoblasts to maintain bone by regulating bone resorption and the coordination of bone matrix synthesis and mineralization, and that this action is most important during times of bone accrual and high rates of bone remodeling.en
dc.language.isoenen
dc.subject.otherAcid Phosphatase.blooden
dc.subject.otherAnimalsen
dc.subject.otherBiological Markers.blooden
dc.subject.otherBone Density.physiologyen
dc.subject.otherBone Remodelingen
dc.subject.otherBone Resorption.blood.metabolism.pathology.physiopathologyen
dc.subject.otherFemur.pathologyen
dc.subject.otherGene Deletionen
dc.subject.otherIntegrases.metabolismen
dc.subject.otherIsoenzymes.blooden
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Knockouten
dc.subject.otherOsteoblasts.metabolismen
dc.subject.otherOsteocalcin.blooden
dc.subject.otherPhenotypeen
dc.subject.otherReceptors, Androgen.metabolismen
dc.subject.otherSpine.metabolism.pathologyen
dc.subject.otherTomography, X-Ray Computeden
dc.titleMineralization and bone resorption are regulated by the androgen receptor in male mice.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Bone and Mineral Researchen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia en
dc.identifier.doi10.1359/jbmr.081217en
dc.description.pages621-31en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/19049333en
dc.type.austinJournal Articleen
local.name.researcherGhasem-Zadeh, Ali
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
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