High fat diet aggravates cardiomyopathy in murine chronic Chagas disease

• Published in: Microbes and infection 2019-01, Vol.21 (1), p.63-71
• Main Authors: Lizardo, Kezia, Ayyappan, Janeesh Plakkal, Cui, Min-Hui, Balasubramanya, Rashmi, Jelicks, Linda A., Nagajyothi, Jyothi F.
• Format: Article
• Language: English
• Subjects: Animals; Chagas Cardiomyopathy - etiology; Chagas Cardiomyopathy - metabolism; Chagas Cardiomyopathy - pathology; Chagas Cardiomyopathy - physiopathology; Chagasic cardiomyopathy; Cholesterol - metabolism; Chronic Disease; Cytokines - metabolism; Diet, High-Fat - adverse effects; Disease Models, Animal; High fat diet; Inflammation; Lipid Metabolism; Liver - metabolism; Male; Mice; Mitochondria, Heart - physiology; Mitochondrial dysfunction; Oxidative Stress; RAGE; Receptor for Advanced Glycation End Products - metabolism; Trypanosoma cruzi - physiology
• ISSN: 1286-4579; 1769-714X
• DOI: 10.1016/j.micinf.2018.07.001

Infection with Trypanosoma cruzi, the etiologic agent in Chagas disease, may result in heart disease. Over the last decades, Chagas disease endemic areas in Latin America have seen a dietary transition from the traditional regional diet to a Western style, fat rich diet. Previously, we demonstrated that during acute infection high fat diet (HFD) protects mice from the consequences of infection-induced myocardial damage through effects on adipogenesis in adipose tissue and reduced cardiac lipidopathy. However, the effect of HFD on the subsequent stages of infection – the indeterminate and chronic stages – has not been investigated. To address this gap in knowledge, we studied the effect of HFD during indeterminate and chronic stages of Chagas disease in the mouse model. We report, for the first time, the effect of HFD on myocardial inflammation, vasculopathy, and other types of dysfunction observed during chronic T. cruzi infection. Our results show that HFD perturbs lipid metabolism and induces oxidative stress to exacerbate late chronic Chagas disease cardiac pathology.