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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/E133    most recent 00354.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Kovacs, C. S. Articles by Friel, J. K. Search for Related Content PubMed PubMed Citation Articles by Kovacs, C. S. Articles by Friel, J. K.

The vitamin D receptor is not required for fetal mineral homeostasis or for the regulation of placental calcium transfer in mice

¹Faculty of Medicine and Endocrinology, ²Department of Biochemistry and Pediatrics, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada

Submitted 3 August 2004 ; accepted in final form 21 February 2005

We utilized a vitamin D receptor (VDR) gene knockout model to study the effects of maternal and fetal absence of VDR on maternal fertility, fetal-placental calcium transfer, and fetal mineral homoeostasis. Vdr null mice were profoundly hypocalcemic, conceived infrequently, and had significantly fewer viable fetuses in utero that were also of lower body weight. Supplementation of a calcium-enriched diet increased the rate of conception in Vdr nulls but did not normalize the number or weight of viable fetuses. Among offspring of heterozygous (Vdr^+/–) mothers (wild type, Vdr^+/–, and Vdr null fetuses), there was no alteration in serum Ca, P, or Mg, parathyroid hormone, placental ⁴⁵Ca transfer, Ca and Mg content of the fetal skeleton, and morphology and gene expression in the fetal growth plates. Vdr null fetuses did have threefold increased 1,25-dihydroxyvitamin D levels accompanied by increased 1-hydroxylase mRNA in kidney but not placenta; a small increase was also noted in placental expression of parathyroid hormone-related protein (PTHrP). Among offspring of Vdr null mothers, Vdr^+/– and Vdr null fetuses had normal ionized calcium levels and a skeletal ash weight that was appropriate to the lower body weight. Thus our findings indicate that VDR is not required by fetal mice to regulate placental calcium transfer, circulating mineral levels, and skeletal mineralization. Absence of maternal VDR has global effects on fetal growth that were partly dependent on maternal calcium intake, but absence of maternal VDR did not specifically affect fetal mineral homeostasis.

fetus; calcitriol; skeletal mineralization; parathyroid hormone-related protein; parathyroid hormone; calbindin-D_9k; calcium-adenosinetriphosphatase; calcium transporter 1 and 2; 1-hydroxylase; placenta

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