Abstract
Empagliflozin enhances human and murine cardiomyocyte glucose uptake by increased expression of GLUT1
Highlights
We have previously reported that empagliflozin improved contractile function in human cardiomyocytes isolated from individuals with heart failure (HF), as well as myocytes from a mouse model of HF by transverse aortic constriction (TAC) [2]
In the present study we investigated whether empagliflozin affects glucose transporter expression and glucose metabolism in cultured murine and human ventricular cardiomyocytes
We report spaghetti graphs for paired data from each specimen to enable better evaluation of the empagliflozin effect. *p
Summary
In the present study we investigated whether empagliflozin affects glucose transporter expression and glucose metabolism in cultured murine and human ventricular cardiomyocytes. Cardiomyocytes were isolated and cultured as described previously [2] (see ESM Methods for details) and exposed to a physiologically relevant concentration of empagliflozin (1 μmol/l [7]) or vehicle control (dimethyl sulfoxide; DMSO). Cell viability after 24 h exposure to empagliflozin was not different from vehicle control and unaffected by treatment with the GLUT inhibitor fasentin (50 μmol/l; ESM Fig. 1).
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