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- W1556570080 abstract "Introduction: In obesity it is unclear how lipid accumulation in the cardiomyocyte contributes to the pathophysiology of metabolic heart disease (MHD). Potential mechanisms of lipid-induced dysfunction include toxic effects or signaling from lipid species and/or increased mitochondrial reactive oxygen species (ROS) production to decrease mitochondrial function. To determine how excess cardiomyocyte lipids mediate MHD, we measured lipid metabolites, lipid sensitive signaling and ROS production in mice with cardiomyocyte-specific overexpression of the fatty acid transport protein-1 (FATP1) in which increased uptake of fatty acids (FA) leads to MHD in the absence of systemic obesity or perturbation of systemic lipid metabolism. Hypothesis: Accumulation of FA in the cardiomyocyte leads to mitochondrial dysfunction and MHD via lipid metabolites and/or mitochondrial oxidant production. Methods and Results: FATP1 and wild type (WT) mice were studied at 5-8 weeks of age. In FATP1 hearts, LC-MS showed increased lo..." @default.
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- W1556570080 date "2014-11-25" @default.
- W1556570080 modified "2023-09-25" @default.
- W1556570080 title "Abstract 18054: Metabolic Remodeling in Mice with Cardiomyocyte-Specific Fatty Acid Overload" @default.
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