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dc.contributor.authorGundberg, Caren M.
dc.contributor.authorLian, Jane B.
dc.contributor.authorBooth, Sarah L.
dc.date2022-08-11T08:10:57.000
dc.date.accessioned2022-08-23T17:26:14Z
dc.date.available2022-08-23T17:26:14Z
dc.date.issued2012-03-01
dc.date.submitted2012-05-10
dc.identifier.citationAdv Nutr. 2012 Mar 1;3(2):149-57. doi: 10.3945/an.112.001834. <a href="http://dx.doi.org/10.3945/an.112.001834">Link to article on publisher's site</a>
dc.identifier.issn2161-8313 (Linking)
dc.identifier.doi10.3945/an.112.001834
dc.identifier.pmid22516722
dc.identifier.urihttp://hdl.handle.net/20.500.14038/49594
dc.description.abstractOsteocalcin originates from osteoblastic synthesis and is deposited into bone or released into circulation, where it correlates with histological measures of bone formation. The presence of 3 vitamin K-dependent gamma carboxyglutamic acid residues is critical for osteocalcin's structure, which appears to regulate the maturation of bone mineral. In humans, the percentage of the circulating osteocalcin that is not gamma-carboxylated (percent ucOC) is used as a biomarker of vitamin K status. In contrast, when ucOC is not corrected for total osteocalcin, the interpretation of this measure is confounded by osteoblastic activity, independent of vitamin K. Observational studies using percent ucOC have led to the conclusion that vitamin K insufficiency leads to age-related bone loss. However, clinical trials do not provide overall support for the suggestion that vitamin K supplementation of the general population will reduce bone loss or fracture risk. More recently, results from in vitro and in vivo studies using animal models indicate that ucOC is an active hormone with a positive role in glucose metabolism. By inference, vitamin K, which decreases ucOC, would have a detrimental effect. However, in humans this hypothesis is not supported by the limited data available, nor is it supported by what has been established regarding osteocalcin chemistry. In summary, the specific function of osteocalcin in bone and glucose metabolism has yet to be elucidated.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22516722&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.3945/an.112.001834
dc.subjectOsteocalcin
dc.subjectVitamin K
dc.subjectCell Biology
dc.titleVitamin k-dependent carboxylation of osteocalcin: friend or foe
dc.typeJournal Article
dc.source.journaltitleAdvances in nutrition (Bethesda, Md.)
dc.source.volume3
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/stein/263
dc.identifier.contextkey2838655
html.description.abstract<p>Osteocalcin originates from osteoblastic synthesis and is deposited into bone or released into circulation, where it correlates with histological measures of bone formation. The presence of 3 vitamin K-dependent gamma carboxyglutamic acid residues is critical for osteocalcin's structure, which appears to regulate the maturation of bone mineral. In humans, the percentage of the circulating osteocalcin that is not gamma-carboxylated (percent ucOC) is used as a biomarker of vitamin K status. In contrast, when ucOC is not corrected for total osteocalcin, the interpretation of this measure is confounded by osteoblastic activity, independent of vitamin K. Observational studies using percent ucOC have led to the conclusion that vitamin K insufficiency leads to age-related bone loss. However, clinical trials do not provide overall support for the suggestion that vitamin K supplementation of the general population will reduce bone loss or fracture risk. More recently, results from in vitro and in vivo studies using animal models indicate that ucOC is an active hormone with a positive role in glucose metabolism. By inference, vitamin K, which decreases ucOC, would have a detrimental effect. However, in humans this hypothesis is not supported by the limited data available, nor is it supported by what has been established regarding osteocalcin chemistry. In summary, the specific function of osteocalcin in bone and glucose metabolism has yet to be elucidated.</p>
dc.identifier.submissionpathstein/263
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages149-57


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