Journal
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
Volume 18, Issue 4, Pages 339-345Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0000000000000188
Keywords
development; epigenetics; intrauterine environment; metabolic syndrome; O-linked N-acetylglucosamine
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Funding
- Intramural Program of the National Institutes of Diabetes, Digestive and Kidney Diseases (NIDDK), National Institutes of Health
- Rotary Foundation Ambassadorial Scholarship from the Rotary Foundation
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Purpose of review The O-linked N-acetylglucosamine (O-GlcNAc) modification is both responsive to nutrient availability and capable of altering intracellular cellular signalling. We summarize data defining a role for O-GlcNAcylation in metabolic homeostasis and epigenetic regulation of development in the intrauterine environment. Recent findings O-GlcNAc transferase (OGT) catalyzes nutrient-driven O-GlcNAc addition and is subject to random X-inactivation. OGT plays key roles in growth factor signalling, stem cell biology, epigenetics and possibly imprinting. The O-GlcNAcase, which removes O-GlcNAc, is subject to tight regulation by higher order chromatin structure. O-GlcNAc cycling plays an important role in the intrauterine environment wherein OGT expression is an important biomarker of placental stress. Summary Regulation of O-GlcNAc cycling by X-inactivation, epigenetic regulation and nutrient-driven processes makes it an ideal candidate for a nutrient-dependent epigenetic regulator of human disease. In addition, O-GlcNAc cycling influences chromatin modifiers critical to the regulation and timing of normal development including the polycomb repression complex and the ten-eleven translocation proteins mediating DNA methyl cytosine demethylation. The pathway also impacts the hypothalamic-pituitary-adrenal axis critical to intrauterine programming influencing disease susceptibility in later life.
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