Review explores the link between glutathione deficiency and immune responses in type 2 diabetes, suggesting implications for treatment.
Glutathione (GSH), a critical antioxidant, plays an essential role in immune function and cellular health. In Type 2 Diabetes Mellitus (T2DM), GSH deficiency exacerbates oxidative stress, impairs immune responses, and increases susceptibility to viral infections, including COVID-19. Chronic hyperglycemia, inflammation, and oxidative damage characteristic of T2DM create a pathological environment that heightens the risk of severe outcomes. This review explores mechanisms linking GSH insufficiency to worsened viral infections, immune dysfunction, and complications such as Acute Respiratory Distress Syndrome (ARDS) and thrombosis. We focus on GSH’s role in SARS-CoV-2 replication and how its deficiency impairs immune defenses, increasing vulnerability in T2DM patients. Potential therapeutic strategies to restore GSH levels, including Nacetylcysteine (NAC) supplementation and liposomal GSH, are discussed. Addressing GSH deficiency may enhance resilience to infections and reduce disease severity in T2DM. By unraveling molecular connections between GSH insufficiency, immune dysfunction, and viral pathogenesis, novel therapies may improve outcomes and mitigate infection severity.
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Yu et al. (2026) studied this question.
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