Abstract
Chagas disease (CD), caused by the protozoan T. cruzi, is a serious public health issue with high morbidity and mortality rates. Approximately 7 million people are infected, mostly in Latin America. The pathogenesis is multifactorial and poorly elucidated, particularly regarding the role of adipose tissue (AT). This review aims to explore the complex relationship between T. cruzi and AT, focusing on the possible role of this tissue in CD, as well as to explore the impact of diet on the progression of the disease. T. cruzi infects adipocytes, affecting their function. Chronic infection alters adipose physiology, contributing to systemic inflammation and metabolic disturbances. Adipokines are dysregulated, while markers of inflammation and oxidative stress increase within AT during CD. Additionally, the immune response and clinical aspects of CD may be influenced by the host's diet. High-fat diets (HFDs) impact parasite burden and cardiac pathology in murine models. The complex interaction among T. cruzi infection, AT dysfunction, and dietary factors underscore the complexity of CD pathogenesis. Despite accumulating evidence suggesting the role of AT in CD, further research is needed to elucidate its clinical implications. Understanding the bidirectional relationship between AT and T. cruzi infection may offer insights into disease progression and potential therapeutic targets, highlighting the importance of considering adipose physiology in CD management strategies.