Chemical hypoxia-induced glucose transporter-4 translocation in neonatal rat cardiomyocytes.
Arch Med Res
; 39(1): 52-60, 2008 Jan.
Article
en En
| MEDLINE
| ID: mdl-18067996
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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas Quinasas
/
Proteínas Serina-Treonina Quinasas
/
Miocitos Cardíacos
/
Transportador de Glucosa de Tipo 4
/
Complejos Multienzimáticos
Límite:
Animals
Idioma:
En
Revista:
Arch Med Res
Asunto de la revista:
MEDICINA
Año:
2008
Tipo del documento:
Article
País de afiliación:
China