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Disordered glycometabolism involved in pathogenesis of Kashin-beck disease, an endemic osteoarthritis in China.
MedLine Citation:
PMID:  24792129     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
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 its effects on KBD chondrocytes. (1)H NMR (nuclear magnetic resonance) 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 an 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 with the damage of chondrocytes. This may provide a new basis for understanding the pathogenesis of KBD.
Authors:
Cuiyan Wu; Ronghui Lei; Mika Tiainen; Shixun Wu; Qiang Zhang; Fuxing Pei; Xiong Guo
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-5-1
Journal Detail:
Title:  Experimental cell research     Volume:  -     ISSN:  1090-2422     ISO Abbreviation:  Exp. Cell Res.     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-5-5     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0373226     Medline TA:  Exp Cell Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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