Gene expression of protein kinase AMP-activated catalytic subunit alpha 1 (PRKAA1), solute carrier family 2 member 1 (SLC2A1) and mechanistic target of rapamycin (MTOR) in metformin-treated type 2 diabetes patients with COVID-19: impact on inflammation markers.
Pavlo PetakhIryna KamyshnaAleksandr KamyshnyiPublished in: Inflammopharmacology (2023)
The COVID-19 pandemic has resulted in a global health crisis that has severely impacted patients with type 2 diabetes (T2D). T2D patients have a higher risk of experiencing severe COVID-19 symptoms, hospitalization, and mortality compared to patients without diabetes. The dysregulated immune response in T2D patients can exacerbate the severity of COVID-19 symptoms. Insulin therapy, a common treatment for T2D patients, has been linked to increased mortality in COVID-19 patients with T2D. However, metformin, an anti-diabetic medication, has been shown to have anti-inflammatory properties that may mitigate the cytokine storm observed in severe COVID-19 cases. In this study, we investigated how the PRKAA1, SLC2A1, and MTOR genes contribute to inflammation markers in COVID-19 patients with T2D, who were receiving either insulin or metformin therapy. Our findings revealed that metformin treatment was associated with reduced expression of genes involved in Th1/Th17 cell differentiation. These results suggest that metformin could be a potential treatment option for T2D patients with COVID-19 due to its anti-inflammatory properties, which may improve patient outcomes.
Keyphrases
- type diabetes
- end stage renal disease
- coronavirus disease
- gene expression
- sars cov
- ejection fraction
- newly diagnosed
- chronic kidney disease
- immune response
- prognostic factors
- peritoneal dialysis
- healthcare
- dna methylation
- protein kinase
- global health
- physical activity
- adipose tissue
- climate change
- risk assessment
- metabolic syndrome
- toll like receptor
- mass spectrometry
- drug induced
- binding protein
- wound healing
- atomic force microscopy
- risk factors