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Article: Glucocorticoid-Induced Osteoporosis in Growing Rats

TitleGlucocorticoid-Induced Osteoporosis in Growing Rats
Authors
KeywordsAnimal model
Glucocorticoid
Osteoporosis
Rats
Issue Date2014
Citation
Calcified Tissue International, 2014, v. 95, n. 4, p. 362-373 How to Cite?
AbstractThis 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.
Persistent Identifierhttp://hdl.handle.net/10722/363205
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 1.016

 

DC FieldValueLanguage
dc.contributor.authorLin, Sien-
dc.contributor.authorHuang, Jianping-
dc.contributor.authorZheng, Liang-
dc.contributor.authorLiu, Yanzhi-
dc.contributor.authorLiu, Guihua-
dc.contributor.authorLi, Nan-
dc.contributor.authorWang, Kuixing-
dc.contributor.authorZou, Liyi-
dc.contributor.authorWu, Tie-
dc.contributor.authorQin, Ling-
dc.contributor.authorCui, Liao-
dc.contributor.authorLi, Gang-
dc.date.accessioned2025-10-10T07:45:11Z-
dc.date.available2025-10-10T07:45:11Z-
dc.date.issued2014-
dc.identifier.citationCalcified Tissue International, 2014, v. 95, n. 4, p. 362-373-
dc.identifier.issn0171-967X-
dc.identifier.urihttp://hdl.handle.net/10722/363205-
dc.description.abstractThis 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.-
dc.languageeng-
dc.relation.ispartofCalcified Tissue International-
dc.subjectAnimal model-
dc.subjectGlucocorticoid-
dc.subjectOsteoporosis-
dc.subjectRats-
dc.titleGlucocorticoid-Induced Osteoporosis in Growing Rats-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00223-014-9899-7-
dc.identifier.pmid25086673-
dc.identifier.scopuseid_2-s2.0-84931042538-
dc.identifier.volume95-
dc.identifier.issue4-
dc.identifier.spage362-
dc.identifier.epage373-
dc.identifier.eissn1432-0827-

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