High fat diet aggravates cardiomyopathy in murine chronic Chagas disease.
Animals
Chagas Cardiomyopathy
/ etiology
Cholesterol
/ metabolism
Chronic Disease
Cytokines
/ metabolism
Diet, High-Fat
/ adverse effects
Disease Models, Animal
Lipid Metabolism
Liver
/ metabolism
Male
Mice
Mitochondria, Heart
/ physiology
Oxidative Stress
Receptor for Advanced Glycation End Products
/ metabolism
Trypanosoma cruzi
/ physiology
Chagasic cardiomyopathy
High fat diet
Inflammation
Lipid metabolism
Mitochondrial dysfunction
RAGE
Journal
Microbes and infection
ISSN: 1769-714X
Titre abrégé: Microbes Infect
Pays: France
ID NLM: 100883508
Informations de publication
Date de publication:
Historique:
received:
13
04
2018
revised:
29
05
2018
accepted:
07
07
2018
pubmed:
3
8
2018
medline:
12
4
2019
entrez:
3
8
2018
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30071300
pii: S1286-4579(18)30146-1
doi: 10.1016/j.micinf.2018.07.001
pmc: PMC6355378
mid: NIHMS1506448
pii:
doi:
Substances chimiques
Ager protein, mouse
0
Cytokines
0
Receptor for Advanced Glycation End Products
0
Cholesterol
97C5T2UQ7J
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
63-71Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL122866
Pays : United States
Informations de copyright
Copyright © 2018 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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