Adenine-induced chronic kidney disease induces a similar skeletal phenotype in male and female C57BL/6 mice with more severe deficits in cortical bone properties of male mice.
Corinne E MetzgerElizabeth A SwallowAlexander J StacyMatthew R AllenPublished in: PloS one (2021)
Chronic kidney disease (CKD) causes bone loss, particularly in cortical bone, through formation of cortical pores which lead to skeletal fragility. Animal models of CKD have shown variability in the skeletal response to CKD between males and females suggesting sex may play a role in this variation. Our aim was to compare the impact of adenine-induced CKD on cortical parameters in skeletally mature male and female C57Bl/6 mice. After 10-weeks of adenine-induced CKD, both male and female adenine mice had high serum parathyroid hormone (PTH), high bone turnover, and cortical porosity compared to non-CKD controls. Both sexes had lower cortical thickness, but only male mice had lower cortical bone area. CKD imparted greater deficits in mechanical properties of male mice compared to female mice. These data demonstrate that both male and female mice develop high PTH/high bone turnover in response to adenine-induced CKD and that cortical bone phenotypes are slightly more severe in males, particularly in mechanical properties deficits.
Keyphrases
- chronic kidney disease
- bone loss
- end stage renal disease
- bone mineral density
- high glucose
- high fat diet induced
- diabetic rats
- traumatic brain injury
- drug induced
- soft tissue
- postmenopausal women
- bone regeneration
- body composition
- machine learning
- early onset
- deep learning
- insulin resistance
- artificial intelligence
- adipose tissue
- metabolic syndrome
- data analysis