Key result
Empagliflozin directly induced upregulation of GLUT1 expression, enhancing glucose uptake and intracellular glucose concentration in isolated failing human and murine cardiomyocytes.
Why the study?
Does empagliflozin enhance glucose uptake in human and murine failing cardiomyocytes?
Does empagliflozin enhance glucose uptake in human and murine failing cardiomyocytes?
p-value: p=<0.05
Empagliflozin enhances glucose uptake in cardiomyocytes via increased GLUT1 expression, providing a potential mechanism for its benefits in heart failure despite the absence of SGLT2 receptors in the myocardium.
Abbreviations 2-DG 2-Deoxyglucose HF Heart failure SGLT2 Sodium-glucose cotransporter 2 TAC Transverse aortic constriction WT Wild-type To the Editor: The results of the Empagliflozin, Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG OUTCOME) showed that the sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin reduced mortality and hospitalisation due to heart failure (HF) in high-risk diabetic patients [1].We have previously reported that empagliflozin improved contractile function in human cardiomyocytes isolated from individuals with HF, as well as myocytes from a mouse model of HF by transverse aortic constriction (TAC) [2].However, we have shown that SGLT2 is not expressed in healthy or failing myocardium.Cardiomyocytes mainly metabolise fatty acids to generate energy for contraction [3].However, HF is characterised by fatty
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Mustroph et al. (2019) conducted a letter in Heart failure. Empagliflozin vs. Vehicle control (DMSO) was evaluated on GLUT1 expression and glucose uptake (p=<0.05). Empagliflozin directly induced upregulation of GLUT1 expression, enhancing glucose uptake and intracellular glucose concentration in isolated failing human and murine cardiomyocytes.
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