Back to Search Start Over

Recovery of the maternal skeleton after lactation is impaired by advanced maternal age but not by reduced IGF availability in the mouse.

Authors :
Rogowska MD
Pena UNV
Binning N
Christians JK
Source :
PloS one [PLoS One] 2021 Sep 01; Vol. 16 (9), pp. e0256906. Date of Electronic Publication: 2021 Sep 01 (Print Publication: 2021).
Publication Year :
2021

Abstract

Background: Lactation results in substantial maternal bone loss that is recovered following weaning. However, the mechanisms underlying this recovery, and in particular the role of insulin-like growth factor 1 (IGF-I), is not clear. Furthermore, there is little data regarding whether recovery is affected by advanced maternal age.<br />Methods: Using micro-computed tomography, we studied bone recovery following lactation in mice at 2, 5 and 7 months of age. We also investigated the effects of reduced IGF-I availability using mice lacking PAPP-A2, a protease of insulin-like growth factor binding protein 5 (IGFBP-5).<br />Results: In 2 month old mice, lactation affected femoral trabecular and cortical bone, but only cortical bone showed recovery 3 weeks after weaning. This recovery was not affected by deletion of the Pappa2 gene. The amount of trabecular bone was reduced in 5 and 7 month old mice, and was not further reduced by lactation. However, the recovery of cortical bone was impaired at 5 and 7 months compared with at 2 months.<br />Conclusions: Recovery of the maternal skeleton after lactation is impaired in moderately-aged mice compared with younger mice. Our results may be relevant to the long-term effects of breastfeeding on the maternal skeleton in humans, particularly given the increasing median maternal age at childbearing.<br />Competing Interests: The authors have declared that no competing interests exist.

Details

Language :
English
ISSN :
1932-6203
Volume :
16
Issue :
9
Database :
MEDLINE
Journal :
PloS one
Publication Type :
Academic Journal
Accession number :
34469481
Full Text :
https://doi.org/10.1371/journal.pone.0256906