Abstract
To the Editor: Poornima et al1 recently reported prolonged survival and preserved ventricular function through chronic treatment with glucagon-like peptide-1 (GLP-1) in spontaneously hypertensive, heart failure-prone rats. The authors explained their findings by insulinotropic effect of GLP-1, that is, augmented insulin secretion causes increased Akt-phosphorylation, consequently reducing cardiomyocyte apoptosis and increasing glucose transporter (GLUT)-4 translocation and myocardial glucose uptake. We believe that some methodological weaknesses question the conclusions and that the results suggest a different mechanism of action. The data on Akt phosphorylation and …
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