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Faculty of Medicine-Endocrinology (J.P.W., C.J.S., N.J.F., C.S.K.), Memorial University of Newfoundland, St. John’s, Newfoundland, Canada A1B 3V6; and University of Texas M.D. Anderson Cancer Research Center (A.O.H., R.F.G.), Houston, Texas 77030
Address all correspondence and requests for reprints to: Dr. Christopher S. Kovacs, Faculty of Medicine-Endocrinology, Memorial University of Newfoundland, 300 Prince Philip Drive, St. John’s, Newfoundland, Canada A1B 3V6. E-mail: ckovacs{at}mun.ca.
The maternal skeleton rapidly demineralizes during lactation to provide calcium to milk, responding to the stimuli of estrogen deficiency and mammary-secreted PTH-related protein. We used calcitonin/calcitonin gene-related peptide-
(Ctcgrp) null mice to determine whether calcitonin also modulates lactational mineral metabolism. During 21 d of lactation, spine bone mineral content dropped 53.6% in Ctcgrp nulls vs. 23.6% in wild-type (WT) siblings (P < 0.0002). After weaning, bone mineral content returned fully to baseline in 18.1 d in Ctcgrp null vs. 13.1 d in WT (P < 0.01) mice. Daily treatment with salmon calcitonin from the onset of lactation normalized the losses in Ctcgrp null mice, whereas calcitonin gene-related peptide- or vehicle was without effect. Compared with WT, Ctcgrp null mice had increased circulating levels of PTH and up-regulation of mammary gland PTH-related protein mRNA. In addition, lactation caused the Ctcgrp null skeleton to undergo more trabecular thinning and increased trabecular separation compared with WT. Our studies confirm that an important physiological role of calcitonin is to protect the maternal skeleton against excessive resorption and attendant fragility during lactation and reveal that the postweaning skeleton has the remarkable ability to rapidly recover even from losses of over 50% of skeletal mineral content.
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