High glucose induces mitochondrial dysfunction independently of protein O-GlcNAcylation

Abstract

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.