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Disordered glycometabolism involved in pathogenesis of Kashin-Beck disease, an endemic osteoarthritis in China.
Exp Cell Res. 2014 Aug 15; 326(2):240-50.EC

Abstract

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.

Authors+Show Affiliations

School of Public Health, Health Science Centre of Xi׳an Jiaotong University, No. 76 Yanta West Road, Xi׳an, Shaanxi 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China; Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi׳an, Shaanxi 710061, PR China. Electronic address: xj.cy.69@stu.xjtu.edu.cn.School of Public Health, Health Science Centre of Xi׳an Jiaotong University, No. 76 Yanta West Road, Xi׳an, Shaanxi 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China; Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi׳an, Shaanxi 710061, PR China. Electronic address: leirh@mail.xjtu.edu.cn.School of Pharmacy, University of Eastern Finland, Kuopio, Finland. Electronic address: mika.tiainen@uef.fi.School of Public Health, Health Science Centre of Xi׳an Jiaotong University, No. 76 Yanta West Road, Xi׳an, Shaanxi 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China; Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi׳an, Shaanxi 710061, PR China. Electronic address: wushixun313@stu.xjtu.edu.cn.Department of Kashin-Beck Disease, Qinghai Institute for Endemic Disease Control and Prevention, Xining, Qinghai 811602, PR China. Electronic address: wdrr@163.com.Department of Orthopedics, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China. Electronic address: peifuxing@vip.163.com.School of Public Health, Health Science Centre of Xi׳an Jiaotong University, No. 76 Yanta West Road, Xi׳an, Shaanxi 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, PR China; Key Laboratory of Trace elements and Endemic Diseases, Ministry of Health, Xi׳an, Shaanxi 710061, PR China. Electronic address: guox@mail.xjtu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24792129

Citation

Wu, Cuiyan, et al. "Disordered Glycometabolism Involved in Pathogenesis of Kashin-Beck Disease, an Endemic Osteoarthritis in China." Experimental Cell Research, vol. 326, no. 2, 2014, pp. 240-50.
Wu C, Lei R, Tiainen M, et al. Disordered glycometabolism involved in pathogenesis of Kashin-Beck disease, an endemic osteoarthritis in China. Exp Cell Res. 2014;326(2):240-50.
Wu, C., Lei, R., Tiainen, M., Wu, S., Zhang, Q., Pei, F., & Guo, X. (2014). Disordered glycometabolism involved in pathogenesis of Kashin-Beck disease, an endemic osteoarthritis in China. Experimental Cell Research, 326(2), 240-50. https://doi.org/10.1016/j.yexcr.2014.04.019
Wu C, et al. Disordered Glycometabolism Involved in Pathogenesis of Kashin-Beck Disease, an Endemic Osteoarthritis in China. Exp Cell Res. 2014 Aug 15;326(2):240-50. PubMed PMID: 24792129.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Disordered glycometabolism involved in pathogenesis of Kashin-Beck disease, an endemic osteoarthritis in China. AU - Wu,Cuiyan, AU - Lei,Ronghui, AU - Tiainen,Mika, AU - Wu,Shixun, AU - Zhang,Qiang, AU - Pei,Fuxing, AU - Guo,Xiong, Y1 - 2014/05/02/ PY - 2013/12/16/received PY - 2014/04/04/revised PY - 2014/04/24/accepted PY - 2014/5/6/entrez PY - 2014/5/6/pubmed PY - 2014/9/27/medline KW - Chondrocyte KW - Glycometabolism KW - Kashin–Beck disease KW - Metabolomics KW - Serum SP - 240 EP - 50 JF - Experimental cell research JO - Exp. Cell Res. VL - 326 IS - 2 N2 - 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. SN - 1090-2422 UR - https://www.unboundmedicine.com/medline/citation/24792129/Disordered_glycometabolism_involved_in_pathogenesis_of_Kashin_Beck_disease_an_endemic_osteoarthritis_in_China_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(14)00177-3 DB - PRIME DP - Unbound Medicine ER -