Chagas disease is currently classified as one of several neglected tropical diseases and as one of the five neglected parasitic infections prioritized by the World Health Organization and the Center for Disease Control for public health intervention. This underscores the fact that the causative agent of American trypanosomiasis has existed for approximately 9.000 years, with positive samples dating back to 7050 B.C. The life cycle of Trypanosoma cruzi (T. cruzi) comprises several morphological transformations involving both mammalian and vector hosts, where three different major developmental stages are identified: epimastigotes, trypomastigotes, and amastigotes. Traditionally, T. cruzi is known to target the heart and gastrointestinal tract; however, its parasitism also results in structural changes and pro-inflammatory effects in adipose tissue and the pancreas.

In this edition of the Arquivos Brasileiros de Cardiologia, a longitudinal study by Barbosa-Ferreira et al. evaluated the levels of insulin, adiponectin, and leptin before and after treatment of acute Chagas disease with benznidazole. Twenty-eight subjects were divided into two groups: a control group (15 subjects) and an acute Chagas disease group (13 subjects). The authors found no significant differences in serum levels of adiponectin and leptin between the groups. In contrast, serum levels of insulin were lower in the acute Chagas group, both before and after treatment, compared to the control group. Additionally, insulin levels were lower in the post-treatment phase compared to the pre-treatment phase.

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