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Authordc.contributor.authorOsorio Fuentealba, César 
Authordc.contributor.authorContreras Ferrat, Ariel Eduardo 
Authordc.contributor.authorAltamirano, Francisco 
Authordc.contributor.authorEspinosa, Alejandra 
Authordc.contributor.authorLi, Qing 
Authordc.contributor.authorNiu, Wenyan 
Authordc.contributor.authorLavandero González, Sergio 
Authordc.contributor.authorKlip, Amira 
Authordc.contributor.authorJaimovich Pérez, Enrique 
Admission datedc.date.accessioned2019-03-15T16:04:24Z
Available datedc.date.available2019-03-15T16:04:24Z
Publication datedc.date.issued2013
Cita de ítemdc.identifier.citationDiabetes, Volumen 62, Issue 5, 2018, Pages 1519-1526
Identifierdc.identifier.issn00121797
Identifierdc.identifier.issn1939327X
Identifierdc.identifier.other10.2337/db12-1066
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/165964
Abstractdc.description.abstractSkeletal 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
Lenguagedc.language.isoen
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceDiabetes
Keywordsdc.subjectInternal Medicine
Keywordsdc.subjectEndocrinology, Diabetes and Metabolism
Títulodc.titleElectrical stimuli release ATP to increase GLUT4 translocation and glucose uptake via PI3Kγ-Akt-AS160 in skeletal muscle cells
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorSCOPUS
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile