title: Glucocorticoid-induced osteoporosis in growing rats.
abstract: This study evaluated whether growing rats were appropriate animal models of glucocorticoid-induced osteoporosis. The 3-month-old male rats were treated with either vehicle or prednisone acetate at 1.5, 3.0, and 6.0 mg/kg/day by oral gavage, respectively. All rats were injected with tetracycline and calcein before sacrificed for the purpose of double in vivo labeling. Biochemistry, histomorphometry, mechanical test, densitometry, micro-CT, histology, and component analysis were performed. We found that prednisone treatments dose dependently decreased body weight, serum biomarkers, biomechanical markers, bone formation, and bone resorption parameters in both tibial and femoral trabecular bone without trabecular bone loss. We also found that significant bone loss happened in femoral cortical bone in the glucocorticoid-treated rats. The results suggested that prednisone not only inhibited bone formation, but also inhibited bone resorption which resulted in poor bone strength but with no cancellous bone loss in growing rats. These data also suggested that the effects of glucocorticoid on bone metabolism were different between cortical bone and trabecular bone, and different between tibia and femur. Growing rats may be a glucocorticoid-induced osteoporosis animal model when evaluated the effects of drugs upon juvenile patients exposed to GC for a long time.
authors.affiliation: Department of Pharmacology, Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College, Zhanjiang, Guangdong, 524023, China.
authors.forename: Sien
authors.initials: S
authors.lastname: Lin
authors.forename: Jianping
authors.initials: J
authors.lastname: Huang
authors.forename: Liang
authors.initials: L
authors.lastname: Zheng
authors.forename: Yanzhi
authors.initials: Y
authors.lastname: Liu
authors.forename: Guihua
authors.initials: G
authors.lastname: Liu
authors.forename: Nan
authors.initials: N
authors.lastname: Li
authors.forename: Kuixing
authors.initials: K
authors.lastname: Wang
authors.forename: Liyi
authors.initials: L
authors.lastname: Zou
authors.forename: Tie
authors.initials: T
authors.lastname: Wu
authors.forename: Ling
authors.initials: L
authors.lastname: Qin
authors.forename: Liao
authors.initials: L
authors.lastname: Cui
authors.forename: Gang
authors.initials: G
authors.lastname: Li
mesh_terms: D000085:Acetates / Q000737:chemistry; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001696:Biomechanical Phenomena; D001835:Body Weight; D001862:Bone Resorption; D003720:Densitometry; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005452:Fluoresceins / Q000737:chemistry; D005938:Glucocorticoids / Q000737:chemistry*; D008297:Male; D010024:Osteoporosis / Q000139:chemically induced / Q000503:physiopathology*; D011241:Prednisone / Q000737:chemistry; D025341:Principal Component Analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical; D013752:Tetracycline / Q000737:chemistry; D013997:Time Factors; D055114:X-Ray Microtomography
chemical_list: D000085:Acetates; D015415:Biomarkers; D005452:Fluoresceins; D005938:Glucocorticoids; D013752:Tetracycline; C007740:fluorexon; D011241:Prednisone