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- W1990486821 abstract "The healthy heart demonstrates remarkable metabolic plasticity. Although it utilizes predominantly fatty acids for ATP generation, it also has the capacity to derive energy from glucose, ketones, lactate, and particular amino acids.1 Such fuel flexibility helps to maintain adequate provision of chemical energy to fuel the unrelenting mechanical work of the heart, especially under conditions of increased physiological or pathological stress. A predominant line of thinking has been that, because of this large energy demand, myocardial metabolic derangements are likely to be causative in heart failure. This seems reasonable because the heart hydrolyzes nearly 20× its mass in ATP each day!1 It is, therefore, reasonable to assume that decrements in ATP production caused by dysregulation of fat or glucose oxidation would promote deleterious changes in cardiac function and structure.Article see p 1022Numerous studies seem to support the concept that metabolism is altered in the failing heart, with a general consensus that, during the course of myocardial remodeling, the heart switches from fatty acid preference to glucose use.2–4 This switch is associated with decreased levels of high energy phosphate reserves,1 suggesting that the failing heart is a fuel-deficient organ. Nevertheless, our understanding of how these metabolic changes occur, when they happen, and to what extent they change is unclear. Even the direction of the changes is still being debated. For example, numerous studies have clearly shown that fat oxidation capacity is decreased in rodent models of heart failure1; yet, the results of clinical studies are variable, showing that fatty acid oxidation in the failing heart is diminished,5 augmented,6–8 or unchanged.9 Although the failing or hypertrophied heart may rely more on glucose metabolism,1 recent studies have shown …" @default.
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- W1990486821 date "2014-11-01" @default.
- W1990486821 modified "2023-10-14" @default.
- W1990486821 title "Insights Into Metabolic Remodeling of the Hypertrophic and Failing Myocardium" @default.
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- W1990486821 doi "https://doi.org/10.1161/circheartfailure.114.001803" @default.
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