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The molecular and cellular processes by which chronic hyperglycemia promotes the development and/or the progression of atherosclerosis, have not been fully elucidated yet. One major hypothesis is that hyperglycemia may cause diabetic vascular complications through the hexosamine pathway. Recent data suggest that glucosamine (GlcNAc), may act by concurrently impairing insulin signal transduction and activating the Endoplasmic Reticulum (ER) stress response in HUVECs. Glucagon-like peptide 1 (GLP-1) analogues-based therapies are a new option for type 2 diabetes treatment. Thus, it’s conceivable that GLP-1 may be able to revert the vicious cycle initiated by glucose toxicity, alleviating ER stress on one side, while on the other enhancing insulin signal transduction improving endothelial function. To verify this hypothesis we will take advantage of an in vitro model of glucose toxicity HUVECs incubated with GlcNAc.
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