Buckle, Kerri Lorraine (2006) Lactational changes in bone metabolism in mice lacking parathyroid hormone (PTH). Masters thesis, Memorial University of Newfoundland.
- Accepted Version
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The female skeleton loses a substantial amount of mineral content during lactation but then is fully restored after weaning. Very little is known about how this is regulated or accomplished. We studied calcium and bone metabolism during pregnancy and lactation in normal mice and in mutants that lack the gene encoding parathyroid hormone (PTH) to determine if PTH is required for the normal accretion of mineral during early pregnancy and the restoration of mineral after weaning. -- We demonstrated that Pth null mothers were hypocalcemic and hyperphosphatemic as compared to normal. Some Pth null mothers had trouble lactating or died under anesthesia; both factors may have been due to hypocalcemia. To address this issue, midway through the project, all mice were placed on a 2% calcium chow instead of the standard 1% calcium chow. All genotypes (wild-type [WT], heterozygous [HET] and Pth null [HOM]) experienced similar gains in bone mineral content (BMC) during pregnancy and lost a comparable amount during lactation regardless of the chow they were fed. For the mice fed the standard chow, all genotypes showed a complete recovery in BMC within three weeks of weaning. -- In summary, these preliminary results suggest that PTH is required for some aspect of normal calcium homeostasis during pregnancy and especially lactation but not to maintain mineral homeostasis and in particular, not to restore skeletal mineral content that was lost during lactation.
|Item Type:||Thesis (Masters)|
|Additional Information:||Includes bibliographical references (leaves 87-95).|
|Department(s):||Medicine, Faculty of|
|Library of Congress Subject Heading:||Calcium--Metabolism--Regulation; Lactation; Parathyroid hormone.|
|Medical Subject Heading:||Calcium--metabolism; Lactation; Parathyroid Hormone.|
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