Chemical Hypoxia-induced Glucose Transporter-4 Translocation in Neonatal Rat Cardiomyocytes

BackgroundAMP-activated protein kinase (AMPK) activation plays an essential role in glucose metabolism of the heart. This study aimed at investigating whether AMPK was involved in glucose transporter-4 (GLUT-4) translocation induced by azide-induced chemical hypoxia in primary cultured neonatal rat cardiomyocytes.MethodsWith or without adenine 9-β-D-arabinofuranoside (ara A, AMPK inbibitor) preincubation, primary cultured rat cardiomyocytes were randomized to several groups as incubated with azide (the respiratory chain inhibitor), insulin, or 5-aminoimidazole-4-carboxyamide-1-β-D-ribofuranoside (AICAR, an AMPK activator). Glucose uptake was measured through γ-scintillation and GLUT-4 protein was detected by Western blot for each group.ResultsAzide-induced chemical hypoxia and AICAR both increased glucose uptake and GLUT-4 translocation in cardiomyocytes, and AICAR had an additive effect on insulin action. Ara A decreased AICAR- and azide-induced glucose uptake and GLUT-4 translocation but did not affect basal or insulin-stimulated glucose uptake.ConclusionsAzide-induced chemical hypoxia increased glucose uptake and GLUT-4 translocation in neonatal rat cardiomyocytes through a mechanism that at least was partially mediated by AMPK activation.