{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Borg DJ"],"funding":["National Health and Medical Research Council","Australian Research Council"],"pagination":["426"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8305727"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(7)"],"pubmed_abstract":["Mechanisms by which advanced glycation end products (AGEs) contribute to type 1 diabetes (T1D) pathogenesis are poorly understood. Since life-long pharmacotherapy with alagebrium chloride (ALT) slows progression to experimental T1D, we hypothesized that acute ALT therapy delivered prediabetes, may be effective. However, in female, non-obese diabetic (NOD<i>ShiLt</i>) mice, ALT administered prediabetes (day 50-100) did not protect against experimental T1D. ALT did not decrease circulating AGEs or their precursors. Despite this, pancreatic β-cell function was improved, and insulitis and pancreatic CD45.1<sup>+</sup> cell infiltration was reduced. Lymphoid tissues were unaffected. ALT pre-treatment, prior to transfer of primed GC98 CD8<sup>+</sup> T cell receptor transgenic T cells, reduced b"],"journal":["Metabolites"],"pubmed_title":["Short Duration Alagebrium Chloride Therapy Prediabetes Does Not Inhibit Progression to Autoimmune Diabetes in an Experimental Model."],"pmcid":["PMC8305727"],"funding_grant_id":["FT110100372","1023664, 1165490, 1084283, 1043315, 1137739, 1004503, 1102935"],"pubmed_authors":["Briskey D","Purcell AW","Forbes JM","Giam KL","McCarthy DA","Ayala R","Scheijen JL","Schalkwijk CG","Faridi P","Dudek NL","Ward MS","Steptoe R","Fotheringham AK","Harcourt BE","Borg DJ","Reeves P","Leung S"],"additional_accession":[]},"is_claimable":false,"name":"Short Duration Alagebrium Chloride Therapy Prediabetes Does Not Inhibit Progression to Autoimmune Diabetes in an Experimental Model.","description":"Mechanisms by which advanced glycation end products (AGEs) contribute to type 1 diabetes (T1D) pathogenesis are poorly understood. Since life-long pharmacotherapy with alagebrium chloride (ALT) slows progression to experimental T1D, we hypothesized that acute ALT therapy delivered prediabetes, may be effective. However, in female, non-obese diabetic (NOD<i>ShiLt</i>) mice, ALT administered prediabetes (day 50-100) did not protect against experimental T1D. ALT did not decrease circulating AGEs or their precursors. Despite this, pancreatic β-cell function was improved, and insulitis and pancreatic CD45.1<sup>+</sup> cell infiltration was reduced. Lymphoid tissues were unaffected. ALT pre-treatment, prior to transfer of primed GC98 CD8<sup>+</sup> T cell receptor transgenic T cells, reduced b","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-04-08T07:30:10.234Z","creation":"2026-04-07T23:42:31.162Z"},"accession":"S-EPMC8305727","cross_references":{"pubmed":["34203471"],"doi":["10.3390/metabo11070426"]}}