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자료유형
학술저널
저자정보
Park So Young (Department of Endocrinology and Metabolism Kyung Hee University Hospital Seoul Korea.) Choi Kyoung Hee (Division of Cardiology Asan Medical Center Seoul Korea.) Jun Ji Eun (Department of Endocrinology and Metabolism Kyung Hee University Hospital at Gangdong Kyung Hee Univ) Chung Ho Yeon (Department of Endocrinology and Metabolism Kyung Hee University Hospital at Gangdong Kyung Hee Univ)
저널정보
대한의학회 Journal of Korean Medical Science Journal of Korean Medical Science Vol.36 No.37
발행연도
2021.9
수록면
1 - 11 (11page)
DOI
10.3346/jkms.2021.36.e239

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Background: Risk of fragility fractures increases in patients with diabetes mellitus, independent of bone mineral density. In the present study, the effects of advanced glycation end products (AGEs) on differentiation and function of osteoblasts and osteoclasts were investigated. Methods: AGEs and 25 mM glucose were administered to marrow-derived macrophages and MCT3T3-E1 cells. The effects of AGEs on osteoclast differentiation was investigated using tartrate-resistant acid phosphatase (TRAP) assay. The effects of AGEs on osteoblast differentiation was investigated using alkaline phosphatase (ALP) activity and bone nodule formation assays. Expression of osteoclast-specific and osteoblast-specific genes and effects on cell signaling pathways associated with cell differentiation were analyzed using reverse transcription polymerase chain reaction and western blotting. Results: AGEs significantly decreased TRAP-positive multinucleated cell formation in receptor activator of nuclear factor-κB ligand-induced marrow-derived macrophages in a dose-dependent manner. AGEs suppressed the expression of osteoclast-specific genes, JNK, p38, AKT, intercellular adhesion molecule 1, and lymphocyte function-associated antigen 1 in marrow-derived macrophages. AGEs decreased ALP activity and showed a tendency to decrease bone nodule formation in MC3T3-E1 cells. AGEs suppressed the expression of osteoblast-specific genes, lysyl hydroxylase and lysyl oxidase in MC3T3-E1 cells. Conclusion: AGEs suppressed differentiation and function of osteoclasts and osteoblasts, and collagen cross-linking activity. It suggests that AGE may induce bone fragility through low bone turnover and deterioration of bone quality

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