The sweet fuel of inflammation: New perspectives on the complex web that interconnects diabetes.

Due to the inflammatory nature of type 2 diabetes mellitus (T2DM) and the increased cardiovascular risk, there is a growing need for innovative strategies to change our identification and treatment approach to avoid clinical complications. One approach would be the use of circulating biomarkers to track disease progression and management. Thus, this study aimed to evaluate the concentrations of inflammatory biomarkers in patients diagnosed with type 2 diabetes mellitus and systemic arterial hypertension, correlating inflammatory cytokines and disease severity. Initially, 259 individuals were stratified into different degrees of disease: low risk, moderate risk, high risk, and very high risk, according to the European Society of Cardiology, which correlates blood pressure values with the presence of cardiovascular risk factors. For this stratification, analysis of body composition, blood pressure measurement, and questionnaires were applied. Blood was collected for biochemical measurements and for ELISA to detect concentrations of cytokines IL-17, IL-1β, IFN-Y, TNF-α, and IL-10. The findings suggest that inflammation is present, contributing to the worsening of systemic arterial hypertension and type 2 diabetes mellitus. Through Bayesian analysis, we found that hyperglycemia plays a role in fueling inflammation, contributing to the maintenance of the state of dysregulation and persistent inflammation, which can contribute to systemic damage. Our work correlates biochemical, glycemic, body composition, blood pressure and inflammatory profiles, showing how they participate together in worsening the prognosis of patients diagnosed with chronic non-communicable diseases. We have seen that all these parameters can be changed with the practice of physical activity, even in conditions of obesity, hyperglycemia or dyslipidemia, when patients do not control the changes with standard pharmacological treatment. Thus, the management measures of these chronic non-communicable diseases must take into account the crosstalk between the systems, and the dysregulation of just one of these systems is enough to generate consequences in all the other systems.