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

ABSTRACT:

Aims

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) improve cardiac performance and clinical outcomes in patients with heart failure, yet mechanisms underlying these beneficial effects remain incompletely understood. We sought to determine whether SGLT2i-induced improvements in cardiac function are dependent on increased cardiac oxidation of ketone bodies.

Methods and results

We employed a mouse model with a cardiac-specific knock-out of the enzyme D-β-hydroxybutyrate dehydrogenase-1 (BDH1^cko), rendering mice incapable of oxidizing the principal ketone body β-hydroxybutyrate in cardiomyocytes. Male BDH1^cko and littermate controls underwent either permanent coronary artery ligation of the left anterior descending coronary artery to induce myocardial

SUBMITTER: Voorrips SN 

PROVIDER: S-EPMC12370586 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature