Journal
CHEMISTRY & BIOLOGY
Volume 17, Issue 9, Pages 949-958Publisher
CELL PRESS
DOI: 10.1016/j.chembiol.2010.07.005
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Funding
- Canadian Institutes for Health Research (CIHR)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Michael Smith Foundation for Health Research (MSFHR)
- Tier II Canada Research Chair in Chemical Biology
- NSERC
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The O-GlcNAc modification is proposed to be a nutrient sensor with studies suggesting that global increases in O-GlcNAc levels cause insulin resistance and impaired glucohomeostasis. We address this hypothesis by using a potent and selective inhibitor of O-GlcNAcase, known as NButGT, in a series of in vivo studies. Treatment of rats and mice with NButGT, for various time regimens and doses, dramatically increases O-GlcNAc levels throughout all tissues but does not perturb insulin sensitivity or alter glucohomeostasis. NButGT also does not affect the severity or onset of insulin resistance induced by a high-fat diet. These results suggest that pharmacological increases in global O-GlcNAc levels do not cause insulin resistance nor do they appear to disrupt glucohomeostasis. Therefore, the protective benefits of elevated O-GlcNAc levels may be achieved without deleteriously affecting glucohomeostasis.
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