<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Teo CF</submitter><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>National Institutes of Health</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>1198-1208</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5884396</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>26(11)</volume><pubmed_abstract>Previous studies utilizing PUGNAc, the most widely used β-N-acetylglucosaminidase (OGA) inhibitor to increase global O-N-acetylglucosamine (GlcNAc) levels, have reported a variety of effects including insulin resistance as a direct result of elevated O-GlcNAc levels. The notion of OGA inhibition causing insulin resistance was not replicated in studies in which elevated global O-GlcNAc levels were achieved using two other OGA inhibitors. Related to insulin action, work by others has suggested that O-GlcNAc elevation may inhibit the anti-apoptotic action of insulin. Thus, we examined the pro-survival action of insulin upon serum deprivation in the presence of PUGNAc as well as two selective OGA inhibitors (GlcNAcstatin-g and Thiamet-G), and a selective lysosomal hexosaminidase inhibitor (INJ</pubmed_abstract><journal>Glycobiology</journal><pubmed_title>Dissecting PUGNAc-mediated inhibition of the pro-survival action of insulin.</pubmed_title><pmcid>PMC5884396</pmcid><funding_grant_id>P41 GM103490</funding_grant_id><funding_grant_id>P41GM103490</funding_grant_id><funding_grant_id>R01DK075069</funding_grant_id><pubmed_authors>El-Karim EG</pubmed_authors><pubmed_authors>Teo CF</pubmed_authors><pubmed_authors>Wells L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dissecting PUGNAc-mediated inhibition of the pro-survival action of insulin.</name><description>Previous studies utilizing PUGNAc, the most widely used β-N-acetylglucosaminidase (OGA) inhibitor to increase global O-N-acetylglucosamine (GlcNAc) levels, have reported a variety of effects including insulin resistance as a direct result of elevated O-GlcNAc levels. The notion of OGA inhibition causing insulin resistance was not replicated in studies in which elevated global O-GlcNAc levels were achieved using two other OGA inhibitors. Related to insulin action, work by others has suggested that O-GlcNAc elevation may inhibit the anti-apoptotic action of insulin. Thus, we examined the pro-survival action of insulin upon serum deprivation in the presence of PUGNAc as well as two selective OGA inhibitors (GlcNAcstatin-g and Thiamet-G), and a selective lysosomal hexosaminidase inhibitor (INJ</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Nov</publication><modification>2025-04-04T19:34:24.203Z</modification><creation>2019-03-26T23:50:11Z</creation></dates><accession>S-EPMC5884396</accession><cross_references><pubmed>27072814</pubmed><doi>10.1093/glycob/cww043</doi></cross_references></HashMap>