Review of the relationship between deficiency of Glucose-6-phosphate dehydrogenase deficiency and diabetes and its complications.

Diabetes is a chronic condition characterised by hyperglycaemia due to impaired insulin secretion, insulin action, or both. Oxidative stress reduces insulin sensitivity and contributes to complications. Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common enzymatic disorder of erythrocytes, impairs NADPH production and reduces the ability to counter oxidative stress. Given the involvement of redox imbalance in diabetes pathogenesis, the role of G6PD deficiency in diabetes development and progression remains unclear. Two reviewers independently searched PubMed, Cochrane Library, and Embase to August 10th, 2026, for primary studies on G6PD deficiency and diabetes, resolving discrepancies by discussion. Forty-two studies met inclusion criteria. G6PD deficiency was more prevalent in T2DM patients than in the general population. Diagnostic complications, including artificially reduced HbA1c, were identified. Specific G6PD variants were associated with increased risk and severity of diabetes-associated retinopathy. G6PD deficiency was also linked to increased risk of myocardial infarction, stroke, and arterial stiffness. Consistent evidence indicates a higher risk of complications associated with G6PD deficiency and diabetes, though associations with diabetes onset remain inconsistent. Future research should investigate genetic stratification, oxidative stress biomarkers, and strategies to reduce morbidity.