Previous reports indicate that hyperglycaemia/diabetes enhances flux through accessory pathways, such as protein O-GlcNAcylation and contributes to cellular dysfunction. In the present study, we examined whether hyperglycaemia induces mitochondrial dysfunction via enhanced protein O-GlcNAcylation. Our results indicate that enhanced protein O-GlcNAcylation does not explain high glucose-induced mitochondrial dysfunction.
High glucose induces mitochondrial dysfunction independently of protein O-GlcNAcylation
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Sujith Dassanayaka, Ryan D. Readnower, Joshua K. Salabei, Bethany W. Long, Allison L. Aird, Yu-Ting Zheng, Senthilkumar Muthusamy, Heberty T. Facundo, Bradford G. Hill, Steven P. Jones; High glucose induces mitochondrial dysfunction independently of protein O-GlcNAcylation. Biochem J 1 April 2015; 467 (1): 115–126. doi: https://doi.org/10.1042/BJ20141018
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