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dc.contributor.authorGonzález-Muñoz, Elena-
dc.contributor.authorLópez-Iglesias, Carmen-
dc.contributor.authorCalvo, María-
dc.contributor.authorPalacín, Manuel-
dc.contributor.authorZorzano, Antonio-
dc.contributor.authorCamps, Marta-
dc.identifierdoi: 10.1210/en.2008-1520-
dc.identifierissn: 0013-7227-
dc.identifiere-issn: 1945-7170-
dc.identifier.citationEndocrinology 150(8): 3493-3502 (2009)-
dc.description.abstractCaveolae are a specialized type of lipid rafts that are stabilized by oligomers of caveolin protein. Caveolae are particularly enriched in adipocytes. Here we analyzed the effects of caveolin-1 knockdown and caveolae ablation on adipocyte function. To this end, we obtained several multiclonal mouse 3T3-L1 cell lines with a reduced expression of caveolin-1 (95% reduction) by a small interfering RNA approach using lentiviral vectors. Control cell lines were obtained by lentiviral infection with lentiviral vectors encoding appropriate scrambled RNAs. Caveolin-1 knockdown adipocytes showed a drastic reduction in the number of caveolae (95% decrease) and cholera toxin labeling was reorganized in dynamic plasma membrane microdomains. Caveolin-1 depletion caused a specific decrease in glucose transporter 4 (GLUT4) and insulin receptor protein levels. This reduction was not the result of a generalized defect in adipocyte differentiation or altered gene expression but was explained by faster degradation of these proteins. Caveolin-1 knockdown adipocytes showed reductions in insulin-stimulated glucose transport, insulin-triggered GLUT4 recruitment to the cell surface, and insulin receptor activation. In all, our data indicate that caveolin-1 loss of function reduces maximal insulin response through lowered stability and diminished expression of insulin receptors and GLUT4. We propose that caveolin-1/caveolae control insulin action in adipose cells. Copyright © 2009 by The Endocrine Society.-
dc.description.sponsorshipE.G.-M. was a Formación de Profesorado Universitario fellow from Ministerio de Educacion y Ciencia (MEC), Spain; M.C. was a Ramón y Cajal researcher from the MEC. This study was supported by research grants from the MEC (BMC2003-07279; BFU2006-13466/BMC; GEN2003-20662-C07), the Generalitat de Catalunya (2005SGR00947), and the Instituto de Salud Carlos III (Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas).-
dc.publisherEndocrine Society-
dc.titleCaveolin-1 loss of function accelerates glucose transporter 4 and insulin receptor degradation in 3T3-L1 adipocytes-
dc.description.versionPeer Reviewed-
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