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Arch Med Res. 2008 Jan;39(1):52-60. Epub 2007 Oct 15.

Chemical hypoxia-induced glucose transporter-4 translocation in neonatal rat cardiomyocytes.

Author information

1
Department of Cardiology, The First Affiliated Hospital, China Medical University, Shenyang, China.

Abstract

BACKGROUND:

AMP-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.

METHODS:

With or without adenine 9-beta-D-arabinofuranoside (ara A, AMPK inhibitor) 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-beta-D-ribofuranoside (AICAR, an AMPK activator). Glucose uptake was measured through gamma-scintillation and GLUT-4 protein was detected by Western blot for each group.

RESULTS:

Azide-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.

CONCLUSIONS:

Azide-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.

PMID:
18067996
DOI:
10.1016/j.arcmed.2007.06.022
[Indexed for MEDLINE]

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