Estradiol-induced regulation of GLUT4 in 3T3-L1 cells: involvement of ESR1 and AKT activation

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dc.citation.issue3
dc.citation.volume59
dc.contributor.authorCampello, Raquel S.
dc.contributor.authorFatima, Luciana A.
dc.contributor.authorBarreto-Andrade, Joao Nilton
dc.contributor.authorLucas, Thais F. [UNIFESP]
dc.contributor.authorMori, Rosana C.
dc.contributor.authorPorto, Catarina S. [UNIFESP]
dc.contributor.authorMachado, Ubiratan F.
dc.coverageBristol
dc.date.accessioned2020-08-04T13:39:57Z
dc.date.available2020-08-04T13:39:57Z
dc.date.issued2017
dc.description.abstractImpaired insulin-stimulated glucose uptake involves reduced expression of the GLUT4 (solute carrier family 2 facilitated glucose transporter member 4, SLC2A4 gene). 17 beta-estradiol (E-2) modulates SLC2A4/GLUT4 expression, but the involved mechanisms are unclear. Although E-2 exerts biological effects by binding to estrogen receptors 1/2 (ESR1/2), which are nuclear transcriptional factorsen
dc.description.abstractextranuclear effects have also been proposed. We hypothesize that E-2 regulates GLUT4 through an extranuclear ESR1 mechanism. Thus, we investigated the effects of E-2 upon (1) subcellular distribution of ESRs and the proto-oncogene tyrosine-protein kinases (SRC) involvementen
dc.description.abstract(2) serine/ threonine-protein kinase (AKT) activationen
dc.description.abstract(3) Slc2a4/GLUT4 expression and (4) GLUT4 subcellular distribution and glucose uptake in 3T3-L1 adipocytes. Differentiated 3T3-L1 adipocytes were cultivated or not with E-2 for 24 h, and additionally treated or not with ESR1-selective agonist (PPT), ESR1-selective antagonist (MPP) or selective SRC inhibitor (PP2). Subcellular distribution of ESR1, ESR2 and GLUT4 was analyzed by immunocytochemistryen
dc.description.abstractSlc2a4 mRNA and GLUT4 were quantified by qPCR and Western blotting, respectivelyen
dc.description.abstractplasma membrane GLUT4 translocation and glucose uptake were analyzed under insulin stimulus for 20 min or not. E-2 induced (1) translocation of ESR1, but not of ESR2, from nucleus to plasma membrane and AKT phosphorylation, effects mimicked by PPT and blocked by MPP and PP2en
dc.description.abstract(2) increased Slc2a4/GLUT4 expression and (3) increased insulin-stimulated GLUT4 translocation and glucose uptake. In conclusion, E-2 treatment promoted a SRC-mediated nucleus-plasma membrane shuttle of ESR1, and increased AKT phosphorylation, Slc2a4/GLUT4 expression and plasma membrane GLUT4 translocationen
dc.description.abstractconsequently, improving insulin-stimulated glucose uptake. These results unravel mechanisms through which estrogen improves insulin sensitivity.en
dc.description.affiliationUniv Sao Paulo, Inst Biomed Sci, Dep Physiol & Biophys, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP (Sao Paulo State Foundation for Research)
dc.description.sponsorshipIDFAPESP: 2012/24210-1
dc.description.sponsorshipIDFAPESP: 2012/04831-1
dc.description.sponsorshipIDFAPESP: 2016/15603-1
dc.format.extent257-268
dc.identifierhttp://dx.doi.org/10.1530/JME-17-0041
dc.identifier.citationJournal Of Molecular Endocrinology. Bristol, v. 59, n. 3, p. 257-268, 2017.
dc.identifier.doi10.1530/JME-17-0041
dc.identifier.issn0952-5041
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57194
dc.identifier.wosWOS:000417615000008
dc.language.isoeng
dc.publisherBioscientifica Ltd
dc.relation.ispartofJournal Of Molecular Endocrinology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectextranuclear ESR1en
dc.subjectSlc2a4en
dc.subjectSRCen
dc.subjectPPTen
dc.subjectMPPen
dc.subjectPP2en
dc.titleEstradiol-induced regulation of GLUT4 in 3T3-L1 cells: involvement of ESR1 and AKT activationen
dc.typeinfo:eu-repo/semantics/article
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