Effects of pregnancy and lactation on maternal bone status in mice artificially selected for larger skeletons

Tran, Vicki

Effects of pregnancy and lactation on maternal bone status in mice artificially selected for larger skeletons

dc.contributor.advisor	Rolian, Campbell Paul
dc.contributor.advisor	Cobb, John Andrew
dc.contributor.author	Tran, Vicki
dc.contributor.committeemember	Manske, Sarah Lynn
dc.contributor.committeemember	Rosa, Brielle Vastola
dc.contributor.committeemember	Gabel, Leigh Elizabeth Christine
dc.date	2023-11
dc.date.accessioned	2023-08-23T19:35:51Z
dc.date.available	2023-08-23T19:35:51Z
dc.date.issued	2023-06
dc.description.abstract	Pregnancy and lactation are intensive physiological processes that require increased calcium demand from the maternal systems. This is mediated by changes to the maternal endocrine axes and may result in excessive bone resorption on the maternal skeleton. Pregnancy- and lactation-related changes in bone have yet to be investigated in a model with poorer bone quality and quantity. The Longshanks mouse (LS) is a mouse line selectively bred for increased tibia length. Although longer, the LS tibia is also weaker due to its altered microarchitecture of thinner and more widely spaced trabeculae. In this study, we sought to investigate the impacts of pregnancy and lactation on maternal bone microarchitecture using the LS as a model of a compromised skeletal phenotype with lower bone quality/quantity. Our study found that LS mice had increased bone quantity at postpartum and substantial decreases at mid-lactation when compared to Controls. The physiological response of increased bone postpartum thus depends on prepregnancy population characteristics and is possibly a mechanism to help protect maternal calcium reserves from excessive depletion. The differences in bone are induced by altered endocrine signaling in LS vs. CTL. The larger improvements in microarchitecture postpartum in the LS may be a result of increased OPG signalling, whereas bone resorption is likely increased in the LS during lactation by PTH and SOST action. This would allow increased mobilization of calcium stores and result in reduced maternal bone quantity/quality as seen in the LS mouse. Overall, this study demonstrated a possible protective response induced by pregnancy, resulting in increased bone volume postpartum, however lactational bone loss should be especially considered in populations with poor bone quality/quantity.
dc.identifier.citation	Tran, V. (2023). Effects of pregnancy and lactation on maternal bone status in mice artificially selected for larger skeletons (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.
dc.identifier.uri	https://hdl.handle.net/1880/116878
dc.identifier.uri	https://dx.doi.org/10.11575/PRISM/41720
dc.language.iso	en
dc.publisher.faculty	Science
dc.publisher.institution	University of Calgary
dc.rights	University of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.
dc.subject	Longshanks
dc.subject	Pregnancy
dc.subject	Lactation
dc.subject	Hormone
dc.subject	Bone
dc.subject.classification	Physiology
dc.title	Effects of pregnancy and lactation on maternal bone status in mice artificially selected for larger skeletons
dc.type	master thesis
thesis.degree.discipline	Biological Sciences
thesis.degree.grantor	University of Calgary
thesis.degree.name	Master of Science (MSc)
ucalgary.thesis.accesssetbystudent	I do not require a thesis withhold – my thesis will have open access and can be viewed and downloaded publicly as soon as possible.