Preserving fatty acid oxidation prevents metabolic shifts toward anabolic pathways, thereby preventing cardiac hypertrophy and improving myocardial energetics.
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FAO preservation may mitigate hypertrophy in animals; leaves open translation to human HF therapies.
Our data show that increased glucose consumption is required to support aspartate synthesis that drives the increase of biomass during cardiac hypertrophy. Preservation of FAO prevents the shift of metabolic flux into the anabolic pathway and maintains catabolic metabolism for energy production, thus preventing cardiac hypertrophy and improving myocardial energetics.
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Ritterhoff et al. (2019) studied this question.
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