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

• Published in: PloS one Vol. 16; no. 4; p. e0250438
• Main Authors: Metzger, Corinne E, Swallow, Elizabeth A, Stacy, Alexander J, Allen, Matthew R
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 23-04-2021; Public Library of Science (PLoS)
• Subjects: Adenine; Aluminum; Anatomy; Anatomy & physiology; Animal models; Biology; Biology and Life Sciences; Biomedical engineering; Bone loss; Chronic kidney failure; Cortical bone; Crystals; Data analysis; Diet; Editing; Females; Fractures; Genetic aspects; Genotype & phenotype; Health care facilities; Kidney diseases; Kidneys; Males; Medicine; Medicine and Health Sciences; Ostomy; Ovariectomy; Parathyroid; Parathyroid hormone; Pathophysiology; Phenotypes; Physical Sciences; Physiological aspects; Physiology; Porosity; Research and Analysis Methods; Sex; Sexes; United States; Indiana; United States > US; Indianapolis Indiana
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0250438

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.