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This Article Full Text Full Text (PDF) All Versions of this Article: 287/2/E218    most recent 00023.2004v1 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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by McDonald, K. R. Articles by Kovacs, C. S. Search for Related Content PubMed PubMed Citation Articles by McDonald, K. R. Articles by Kovacs, C. S.

Ablation of calcitonin/calcitonin gene-related peptide- impairs fetal magnesium but not calcium homeostasis

¹Faculty of Medicine - Endocrinology, Memorial University of Newfoundland, St. John's, Newfoundland A1B 3V6; ²Department of Biochemistry and Pediatrics, Memorial University of Newfoundland, St. John's, Newfoundland A1B 3X9, Canada; and ³University of Texas MD Anderson Cancer Research Center, Houston, Texas 77030

Submitted 16 January 2004 ; accepted in final form 18 March 2004

We used the calcitonin/calcitonin gene-related peptide (CGRP)- gene knockout model (Ct/Cgrp null) to determine whether calcitonin and CGRP are required for normal fetal mineral homeostasis and placental calcium transfer. Heterozygous (Ct/Cgrp^+/–) and Ct/Cgrp null females were mated to Ct/Cgrp^+/– males. One or two days before term, blood was collected from mothers and fetuses and analyzed for ionized Ca, Mg, P, parathyroid hormone (PTH), and calcitonin. Amniotic fluid was collected for Ca, Mg, and P. To quantify skeletal mineral content, fetuses were reduced to ash, dissolved in nitric acid, and analyzed by atomic absorption spectroscopy for total Ca and Mg. Placental transfer of ⁴⁵Ca at 5 min was assessed. Ct/Cgrp null mothers had significantly fewer viable fetuses in utero compared with Ct/Cgrp^+/– and wild-type mothers. Fetal serum Ca, P, and PTH did not differ by genotype, but serum Mg was significantly reduced in null fetuses. Placental transfer of ⁴⁵Ca at 5 min was normal. The calcium content of the fetal skeleton was normal; however, total Mg content was reduced in Ct/Cgrp null skeletons obtained from Ct/Cgrp null mothers. In summary, maternal absence of calcitonin and CGRP reduced the number of viable fetuses. Fetal absence of calcitonin and CGRP selectively reduced serum and skeletal magnesium content but did not alter ionized calcium, placental calcium transfer, and skeletal calcium content. These findings indicate that calcitonin and CGRP are not needed for normal fetal calcium metabolism but may regulate aspects of fetal Mg metabolism.

fetus; placental calcium transfer; skeletal mineralization; mineral homeostasis