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Glucotoxicity is mediated at least in part by accumulation of excess ROS generated by several metabolic pathways, including mitochondrial oxidative phosphorylation and other alternative metabolic pathways, such as glucose autoxidation, hexosamine metabolism, sorbitol metabolism, and increased protein glycation (120, 121)

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The equality of baseline data among the study groups was assessed using the Kruskal–Wallis test for numeric variables and the Pearson chi-square test for nominal variables