Chronic Trypanosoma cruzi infection potentiates adipose tissue macrophage polarization toward an anti-inflammatory M2 phenotype and contributes to diabetes progression in a dietinduced obesity model

ONCOTARGET

LLC IMPACT JOURNALS

Lugar: New York; Año: 2016 vol. 7 p. 13400 - 13400

hronic obesity and Chagas disease (caused by the protozoan Trypanosomacruzi) represent serious public health concerns. The interrelation between parasiteinfection, adipose tissue, immune system and metabolism in an obesogenic context,has not been entirely explored. A novel diet-induced obesity model (DIO) wasdeveloped in C57BL/6 wild type mice to examine the effect of chronic infection(DIO+I) on metabolic parameters and on obesity-related disorders. Dyslipidemia,hyperleptinemia, and cardiac/hepatic steatosis were strongly developed in DIOmice. Strikingly, although these metabolic alterations were collectively improvedby infection, plasmatic apoB100 levels remain significantly increased in DIO+I,suggesting the presence of pro-atherogenic small and dense LDL particles. Moreover,acute insulin resistance followed by chronic hyperglycemia with hypoinsulinemiawas found, evidencing an infection-related-diabetes progression. These lipid andglucose metabolic changes seemed to be highly depende