Original article
Effects of -blockers on -adrenergic receptor (AR)-mediated insulin resistance in
neonatal rat cardiomyocyte
Sarawuth Phosri1,*, Darawan Pinthong2, Supachoke Mangmool1
1
Department of Pharmacology, Faculty of Pharmacy; 2Department of Pharmacology,
Faculty of Science, Mahidol University, Bangkok 10400, Thailand
E-mail: aonsungphar@gmail.com
Abstract
Insulin resistance is characterized by the reduced ability of insulin to stimulate the uptake of
glucose by many tissues including cardiac muscle which is associated with inflammation,
oxidative stress and myocardial remodeling. It is noteworthy that some of these conditions
are characterized by dysregulation of the sympathetic nervous system, resulting in enhanced
stimulation of βAR. Due to overstimulation of βAR causes insulin resistance, we hypothesize
that β-blockers may suppress the βAR-induced insulin resistance in heart. Therefore, we will
investigate determine whether β-blockers effect on the βAR-induced insulin resistance
focusing on insulin-induced glucose uptake, glucose transporter 4 (GLUT4) expression and
GLUT4 translocation. This study reported that propranolol and metoprolol significantly
antagonized the inhibitory effect of isoproterenol (ISO; βAR agonist) on insulin-induced
glucose uptake, whereas atenolol tend to inhibit the effect of ISO in neonatal rat
cardiomyocytes. In addition, propranolol is able to antagonize the action of ISO- mediated
inhibition of insulin-induced GLUT4 mRNA expression, whereas atenolol, metoprolol and
propranolol are able to suppress the effect of ISO-mediated inhibition of insulin-induced
GLUT4 translocation in neonatal rat cardiomyocytes. Thus, this study suggests that using of
these β-blockers might have the potential benefit on patients which found insulin resistance
inducing by the sympathetic overactivation in the heart.
Keywords: β-adrenergic receptor (βAR), cardiomyocytes, GLUT4 translocation, glucose
uptake, insulin resistance