Empagliflozin Repurposing for Metabolic Substrate Switching and Ketogenesis
Abstract
Empagliflozin promotes glucose excretion via SGLT2 inhibition, forcing metabolic shift toward ketone body utilization which bypasses fatty acid β-oxidation defects. The drug upregulates hepatic ketogenesis through FGF21 signaling and enhances cardiac and skeletal muscle ketone oxidation via increased expression of ketone body transporters MCT1 and MCT2.
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