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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAQYGdRveClO2vxe8FxG4oB8XBY_UNod-PATCaKETyXOA#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAQYGdRveClO2vxe8FxG4oB8XBY_UNod-PATCaKETyXOA#_5 http://www.w3.org/ns/prov#value The ability of a variety of nutrients to activate the hexosamine pathway has led to the theory that this pathway serves as a general nutrient sensing pathway, through which hyperglycemia or hyperlipidemia could decrease insulin sensitivity of cells when nutrient excess prevails (148). In cell culture, omission of glutamine (a cofactor of GFA) from the media, or addition of glutamine analogues, blunts the desensitizing effect of glucose on insulin sensitivity (150). Glucosamine infusion for two to six hours will decrease insulin-stimulated IRS-1 tyrosine phosphorylation, PI3-kinase activation, and activation of glycogen synthase in a manner that parallels the decrease in insulin-stimulated glucose uptake in skeletal muscle. 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