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During heart failure, mitochondrial oxidative capacity is reduced by increased reactive oxygen species (ROS), dysregulated mitochondrial Ca 2+ homeostasis, impaired mitochondrial dynamics, mitochondrial autophagy and other adverse factors, leading to a reduced capacity and efficiency of fatty acid and glucose oxidation ( Many studies support the concept that ketones are alternative metabolic substrates for failing hearts

Oleylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-alpha

3(5): 34560 Pearson DJ, Tubbs PK, Chase JF

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