PRRT2 and Hyperglycemia: Recent studies using isotopic tracer techniques have quantified the relative contributions of these pathways, revealing that mitochondrial O2•− production initiates about 45% of hyperglycemia-induced damage, while PKC activation and AGE formation account for 30% and 25%, respectively (Chronic Complications of Diabetes Mellitus, 2024; Pardina et al., 2024).