Artículos de revistas
Electrical stimuli release ATP to increase GLUT4 translocation and glucose uptake via PI3Kγ-Akt-AS160 in skeletal muscle cells
Fecha
2013Registro en:
Diabetes, Volumen 62, Issue 5, 2018, Pages 1519-1526
00121797
1939327X
10.2337/db12-1066
Autor
Osorio Fuentealba, César
Contreras Ferrat, Ariel Eduardo
Altamirano, Francisco
Espinosa, Alejandra
Li, Qing
Niu, Wenyan
Lavandero González, Sergio
Klip, Amira
Jaimovich Pérez, Enrique
Institución
Resumen
Skeletal muscle glucose uptake in response to exercise is preserved in insulin-resistant conditions, but the signals involved are debated. ATP is released from skeletal muscle by contractile activity and can autocrinely signal through purinergic receptors, and we hypothesized it may influence glucose uptake. Electrical stimulation, ATP, and insulin each increased fluorescent 2-NBD-Glucose (2-NBDG) uptake in primary myotubes, but only electrical stimulation and ATP-dependent 2-NBDG uptake were inhibited by adenosine-phosphate phosphatase and by purinergic receptor blockade (suramin). Electrical stimulation transiently elevated extracellular ATP and caused Akt phosphorylation that was additive to insulin and inhibited by suramin. Exogenous ATP transiently activated Akt and, inhibiting phosphatidylinositol 3-kinase (PI3K) or Akt as well as dominant-negative Akt mutant, reduced ATP-dependent 2-NBDG uptake and Akt phosphorylation. ATP-dependent 2-NBDG uptake was also inhibited by the G prot