Exploring the Warburg effect in Chagas disease: A biochemical approach to metabolic reprogramming.

Chagas disease (CD), caused by Trypanosoma cruzi, is a significant problem of public health. The infection induces inflammatory processes in tissues, leading to metabolic changes similar to the Warburg Effect (WE). To evaluate the presence of WE during the progression of CD in mice, 72 male Swiss mice were divided in two groups: one group with 36 mice was infected with 5.0 × 10⁴ trypomastigote forms of T. cruzi QM2 strain, and another group with 36 mice was the control. Every week the mice were weighed, glycemia was measured and lactate was determined biweekly. At the end of each experimental period: 30, 60 and 120 days post-infection, the animals were euthanized for blood collection to analyze TBARS, LDH, urea, creatinine, PCR, pO2 and pCO2. Parasitemic peak was reached in 17th day, when blood glucose was lowered. Glycemia was significantly lower in the infected group, with high lactate dehydrogenase (LDH) activity, suggesting the occurrence of WE, despite normal lactate and pH levels in this group. Neither TBARS nor C-reactive protein showed significant difference across the groups studied. Urea levels did not show significant differences between the groups, but the decrease in its concentration in the infected group may be due to the use of its precursors for the production of nitric oxide. It is concluded that hypoglycemia and increased LDH activity during the acute phase of CD led to a metabolic shift towards glycolysis, suggesting the presence of WE. Further studies are necessary to validate this metabolic shift in CD.