As the main underlying mechanism for the insulin resistance profile, it has been proposed that T. cruzi persistence in adipose tissue induces the adoption of a pro-inflammatory phenotype responsible for the metabolic disturbances that include increased production of pro-inflammatory cytokines (i.e., IL-6, MCP-1, TNF-α), inhibition of PPAR-γ pathway and diminished adiponectin synthesis with higher resistin systemic levels [16,17,32,33]. This evidence concerns the gene RETN and Insulin resistance.