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Disordered glycometabolism involved in pathogenesis of Kashin-Beck disease, an endemic osteoarthritis in China.

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机构: [1]School of Public Heath, Health Science Centre of Xi'an Jiaotong University, No.76 Yanta West Road, Xian, Shanxi 710061,PR China [2]Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China [3]Key Laboratory of Trace elements and Endemic Diseases,Ministry of Health, Xi'an, Shaanxi 710061, PR China [4]school of Pharmacy,University of Eastern Finland, Kuopio,Finland [5]Department of Kashin-Beck Disease, Qinghai lnstitute for Endemic Disease Control and Prevention, Xining.Qinghai 811602,PR China [6]Department of Orthopedics, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China
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关键词: Kashin–Beck disease Metabolomics Serum Chondrocyte Glycometabolism

摘要:
Kashin-Beck disease (KBD) is a chronic endemic osteoarthritis in China. Previous studies have suggested a role of metabolic dysfunction in causation of this disease. In this investigation, the metabolomics approach and cell experiments were used to discover the metabolic changes and their effects on KBD chondrocytes. Nuclear magnetic resonance ((1)H NMR) spectroscopy was used to examine serum samples from both the KBD patients and normal controls. The pattern recognition multivariate analysis (OSC-PLS) and quantitative analysis (QMTLS iterator) revealed altered glycometabolism in KBD, with increased glucose and decreased lactate and citrate levels. IPA biological analysis showed the centric location of glucose in the metabolic network. Massive glycogen deposits in chondrocytes and increased uptake of glucose by chondrocytes further confirmed disordered glycometabolism in KBD. An in vitro study showed the effects of disordered glycometabolism in chondrocytes. When chondrocytes were treated with high glucose, expression of type II collagen and aggrecan were decreased, while TNF-α expression, the level of cellular reactive oxygen species and cell apoptosis rates all were increased. Therefore, our results demonstrated that disordered glycometabolism in patients with KBD was linked to the damage of chondrocytes. This may provide a new basis for understanding the pathogenesis of KBD. Copyright © 2014 Elsevier Inc. All rights reserved.

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出版当年[2014]版:
大类 | 3 区 医学
小类 | 3 区 肿瘤学 4 区 细胞生物学
最新[2023]版:
大类 | 3 区 生物学
小类 | 4 区 细胞生物学 4 区 肿瘤学
第一作者:
第一作者机构: [1]School of Public Heath, Health Science Centre of Xi'an Jiaotong University, No.76 Yanta West Road, Xian, Shanxi 710061,PR China [2]Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China [3]Key Laboratory of Trace elements and Endemic Diseases,Ministry of Health, Xi'an, Shaanxi 710061, PR China
通讯作者:
通讯机构: [1]School of Public Heath, Health Science Centre of Xi'an Jiaotong University, No.76 Yanta West Road, Xian, Shanxi 710061,PR China [2]Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China [3]Key Laboratory of Trace elements and Endemic Diseases,Ministry of Health, Xi'an, Shaanxi 710061, PR China [*1]School of Public Health, Health Science Centre of Xi'an Jiaotong University, No 76 Yanta West Road, Xi'an, Shaanxi 710061, PR China
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