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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 저널정보
- 한국응용약물학회 한국응용약물학회 추계학술발표논문집 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
- 발행연도
- 2003.1
- 수록면
- 79 - 79 (1page)
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초록· 키워드
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Recently diabetes has been found to be associated with metabolic bone diseases such as osteoporosis. In the present study, attempts have been made-to explore the effect of high glucose in bone formation. Osteoblast-like UMR 106 cells were treated with high glucose (22mM, 33mM, 44mM) for 1 or 2 days. High glucose significantly inhibited proliferation of UMR106 cells in a time- and dose- dependent manner as evidenced by MTT assay. For the evaluation of collagen synthesis, UMR 106 cells were cultured in high glucose media (44mM) for 24 h and the ratio of collagen content to total protein was measured. In addition, gene expression pattern of type I collagen was assessed by RT-PCR. The high concentration of glucose inhibited a collagen synthesis, a marker of bone formation activity. JNK, c- Jun N-terminal Kinase, is known to play an important role in stress-associated cell death. In this regard, we tested to determine whether high glucose has any effect on JNK activity. It has been found that treatment of high glucose induced phosphorylation of JNK. On the other hand, ERK phosphorylation was inhibited by high glucose in a dose-dependent manner. Taken together, Therefore these results indicate that inhibition of proliferation in UMR 106 cells following high glucose is related to JNK/ERK containing signal pathways. This study showed high glucose concentration could alter the bone metabolism leading to defective bone formation, suggesting that high glucose due to diabetes may playa significant role in the development of metabolic bone disease.
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