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Free Radic Res. 2016 Oct;50(10):1080-1088. Epub 2016 Oct 19.

The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome.

Author information

1
a Center for Mitochondrial Biology and Medicine, the Key Laboratory of Biomedical Information Engineering of Ministry of Education , School of Life Science and Technology and Frontier Institute of Science and Technology, Xi'an Jiaotong University , Xi'an , China.
2
b Section of Comparative Medicine and Department of Cellular and Molecular Physiology , Yale University School of Medicine , New Haven , CT , USA.

Abstract

Nutrients excess is one of the leading causes of metabolic syndrome globally. Protein post-translational O-GlcNAc modification has been recognized as an essential nutrient sensor of the cell. Emerging studies suggest that O-GlcNAcylation lies at the core linking nutritional stress to insulin resistance. Mitochondria are the major site for ATP production in most eukaryotes. Mitochondrial dysfunction and oxidative stress have long been considered as an important mechanism underlying insulin resistance. The metabolic process is under the influence of environmental and nutritional factors, thus sensing and transducing nutritional signals sit at the pivot of metabolism control. For a long time little was known about O-GlcNAcylation within mitochondria since mitochondrial O-GlcNAcylation was regarded rare. Recent findings have demonstrated that O-GlcNAcylation is widely spread among mitochondrial proteins, and that mitochondrial function and oxidative stress both can be regulated by O-GlcNAcylation, particularly under diabetic circumstances.

KEYWORDS:

O-GlcNAcylation; insulin resistance; mitochondria; nutrient sensing; oxidative stress

PMID:
27646831
PMCID:
PMC5466075
DOI:
10.1080/10715762.2016.1239017
[Indexed for MEDLINE]
Free PMC Article

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