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dc.contributor.authorJorde, Rolf
dc.contributor.authorStunes, Astrid Kamilla
dc.contributor.authorKubiak, Julia Magdalena
dc.contributor.authorJoakimsen, Ragnar Martin
dc.contributor.authorGrimnes, Guri
dc.contributor.authorThorsby, Per Medbøe
dc.contributor.authorSyversen, Unni
dc.date.accessioned2019-12-17T14:55:24Z
dc.date.available2019-12-17T14:55:24Z
dc.date.issued2019-04-05
dc.description.abstractIn observational studies, vitamin D deficiency is a risk factor for low bone density and future fractures, whereas a causal relation has been difficult to show in randomized controlled trials (RCTs). Similarly, vitamin D deficiency has been associated with increased bone turnover, but RCTs with vitamin D have not shown conclusive effects. This could be due to inclusion of vitamin D sufficient subjects and low vitamin D doses. In the present study 399 subjects with mean baseline serum 25-hydroxyvitamin D (25(OH)D) 34.0 nmol/L completed a four months intervention with vitamin D<sub>3</sub> 20,000 IU per week versus placebo. Mean serum 25(OH)D increased to 89.0 nmol/L in the vitamin D group and decreased slightly in the placebo group. A small, but significant, decrease in the bone formation marker procollagen of type 1 amino-terminal propeptide (P1NP) was seen in the vitamin D group as compared to the placebo group (mean delta P1NP -1.2 pg/mL and 1.5 ng/mL, respectively, P < 0.01). No significant effects were seen on serum carboxyl-terminal telopeptide of type 1 collagen (CTX-1), Dickkopf-1, sclerostin, tumor necrosis factor-alpha, osteoprotegerin, receptor activator of nuclear factor ĸB ligand, or leptin. Subgroup analyses on subjects with low baseline serum 25(OH)D did not yield additional, significant results. In subjects with high baseline serum parathyroid hormone (PTH) > 6.5 pmol/L and post-intervention decrease in PTH, the decrease in P1NP was more pronounced, they also exhibited significantly reduced serum CTX-1 and increased serum sclerostin. In conclusion, supplementation with vitamin D appears to suppress bone turnover, possibly mediated by PTH reduction. Our findings need to be confirmed in even larger cohorts with vitamin D insufficient subjects.en_US
dc.identifier.citationJorde r, Stunes AK, Kubiak JM, Joakimsen RM, Grimnes G, Thorsby PM, Syversen U. Effects of vitamin D supplementation on bone turnover markers and other bone-related substances in subjects with vitamin D deficiency. Bone. 2019;124:7-13en_US
dc.identifier.cristinIDFRIDAID 1691344
dc.identifier.doi10.1016/j.bone.2019.04.002
dc.identifier.issn8756-3282
dc.identifier.issn1873-2763
dc.identifier.urihttps://hdl.handle.net/10037/16960
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.relation.journalBone
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright The Author(s).
dc.subjectVDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710en_US
dc.subjectVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710en_US
dc.titleEffects of vitamin D supplementation on bone turnover markers and other bone-related substances in subjects with vitamin D deficiencyen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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