Myocardial ketone body oxidation contributes to empagliflozin-induced improvements in cardiac contractility in murine heart failure.

Although the increase in tissue β‐hydroxybutyrate levels did not reach statistical significance, the observed trend suggests a potential accumulation. β‐hydroxybutyrate has been previously shown to mitigate the development of cardiac hypertrophy in response to pathological stress. 15 , 27 This effect is likely mediated by the posttranslational effects of β‐hydroxybutyrate.

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