The COVID-19 pandemic has left a lasting impact on the global population, and although it has officially been declared over, the emergence of new variants such as JN.1 continues to pose threats. Among the various risk factors associated with severe outcomes, type 2 diabetes (T2D) has been a major concern. However, recent research conducted by experts from Uzhhorod National University, I. Horbachevsky Ternopil National Medical University, and the University of Bergen has shed light on the potential benefits of metformin, a primary treatment for T2D, in COVID-19 patients with T2D.
Metformin is primarily known for its role in glycemic control, but it has been found to have pleiotropic effects that extend beyond its glucose-lowering properties. One of the key mechanisms behind these benefits is metformin’s ability to reduce inflammation. By influencing the immunometabolism of lymphocytes, metformin can impact the balance between pro-inflammatory and anti-inflammatory T cells. This modulation has the potential to decrease inflammation and lower the risk of severe cases of COVID-19.
Maintaining immune homeostasis is crucial for a well-balanced immune response. In the context of COVID-19, an imbalance in the activation of T-lymphocyte subpopulations can contribute to the severity of the disease. The study focused on the expression levels of three genes involved in the transcriptional regulation of T cells and found that individuals who were not taking metformin exhibited altered expression levels of these genes. In contrast, metformin-treated individuals displayed a more balanced expression pattern, suggesting that the medication may have a regulatory effect on immune responses.
The composition of gut microbiota plays a significant role in both T2D and COVID-19. Metformin has been shown to have beneficial effects on gut microbiota in patients with both conditions. The medication promotes the growth of beneficial bacteria and reduces pro-inflammatory cytokine levels in the gut. This dual effect could contribute to improved outcomes in COVID-19 patients with T2D by reducing both lung and systemic inflammation.
The study revealed that individuals treated with metformin exhibited a more favorable T-lymphocyte gene expression profile and a positive correlation between gut microbiota imbalance and T-cell subset dysregulation. Metformin-treated individuals also showed lower inflammatory markers and higher gut microbiota diversity, aligning with previous studies demonstrating the medication’s anti-inflammatory and microbiota-modulating effects.
While the study provides valuable insights into the molecular changes induced by metformin, it acknowledges limitations such as a small sample size and reliance on culture-based microbiota analysis. Further research using advanced sequencing techniques and larger cohorts is necessary to validate and refine these observations.
In conclusion, the study highlights the potential of metformin to influence immune response genes and modulate gut microbiota in COVID-19 patients with T2D. The observed upregulation of anti-inflammatory markers and downregulation of pro-inflammatory markers in metformin-treated individuals suggest a beneficial impact. However, cautious interpretation is warranted, and further research is needed to solidify metformin’s role in immune modulation during COVID-19. These findings offer a promising foundation for future clinical applications and therapeutic strategies, emphasizing metformin as a potential ally in the fight against severe outcomes in COVID-19 patients with T2D.