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Calcitonin Plays a Critical Role in Regulating Skeletal Mineral Metabolism during Lactation
Abstract
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-alpha (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-alpha 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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“Injection of sCT normalized the bone parameters, whereas CGRP was without effect, indicating that calcitonin is the peptide that plays an important role in calcium balance and preservation of the maternal skeleton during lactation and its recovery after weaning (222).”
From The Activity of Peptides of the Calcitonin Family in Bone (2019) · cites this paper as [222]
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“Thirteen days after weaning, spine bone mineral content returned to baseline values in the WT mice, whereas in the Calca KO mice, it took 18 days to reach these values.”
From The Activity of Peptides of the Calcitonin Family in Bone (2019) · cites this paper as [222]
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“In the Calca KO model, deficient in both calcitonin and CGRP, spine bone mineral content dropped during 21 days of lactation by over 50%, whereas in the WT controls, the drop was only of 23.6% (222).”
From The Activity of Peptides of the Calcitonin Family in Bone (2019) · cites this paper as [222]
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Metadata
- Authors
- Woodrow, J. P., Sharpe, C. J., Fudge, N. J., Hoff, A. O., Gagel, R. F., & Kovacs, C. S.
- Affiliations
- Memorial University of Newfoundland (CA)
- The University of Texas MD Anderson Cancer Center (US)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2006-09
- Volume
- 147
- Issue
- 9
- Pages
- 4010-4021
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2038783196
- Cited by
- 195
- References
- 70
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 13 · 2023: 6 · 2022: 5 · 2021: 12 · 2020: 14 · 2019: 11 · 2018: 7 · 2017: 16 · 2016: 9 · 2015: 7 · 2014: 10 · 2013: 9 · 2012: 16
- FWCI
- 10.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Society for Endocrinology
- Memorial University of Newfoundland
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- calcitonin, lactation, bone demineralization, salmon calcitonin, PTH-related protein, parathyroid hormone, estrogen deficiency, trabecular bone, bone mineral content
- MeSH terms
- Animals, Biomechanical Phenomena, Bone and Bones, Bone Diseases, Metabolic, Bone Resorption, Calcitonin, Calcium, Duodenum, Estradiol, Female, Intestinal Absorption, Lactation, Mammary Glands, Animal, Milk, Minerals, Parathyroid Hormone, Pregnancy, RNA, Messenger, Bone Density, Calcitonin Gene-Related Peptide, Mice, Knockout, Parathyroid Hormone-Related Protein, Mice
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