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.
- hexosamine biosynthetic pathway
- mitochondrial function
Abbreviations: (m)OGA, mitochondrial OGA; (m)OGT, mitochondrial OGT; AA, antimycin A; Ad-Null, null adeno virus; Ad-OGA, adenoviruses carrying OGA gene; Ad-OGT, adenoviruses carrying OGT gene; DMEM, Dulbecco's modified Eagle's medium; HBP, hexosamine biosynthetic pathway; MAS, mannitol and sucrose; NRCM, neonatal rat cardiomyocyte; OCR, oxygen consumption rate; OGA, O-GlcNAcase; O-GlcNAc, β-O-linked-N-acetylglucosamine; OGT, O-GlcNAc transferase; Rot, rotenone; TMG, Thiamet G; XF, extracellular flux
- © The Authors Journal compilation © 2015 Biochemical Society