Glucose in chronic excess causes toxic effects on structure and function of organs, including
the pancreatic islet. Multiple biochemical pathways and mechanisms of action for glucose
toxicity have been suggested. These include glucose autoxidation, protein kinase C
activation, methylglyoxal formation and glycation, hexosamine metabolism, sorbitol
formation, and oxidative phosphorylation. There are many potential mechanisms whereby
excess glucose metabolites traveling along these pathways might cause beta cell damage …