Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/56076
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dc.contributor.authorMiana, María-
dc.contributor.authorGalán, María-
dc.contributor.authorMartínez-Martínez, Ernesto-
dc.contributor.authorVarona, Saray-
dc.contributor.authorJurado-López, Raquel-
dc.contributor.authorBausa-Miranda, Belén-
dc.contributor.authorantequera, alfonso-
dc.contributor.authorLuaces, María-
dc.contributor.authorMartínez-González, José-
dc.contributor.authorRodríguez, Cristina-
dc.contributor.authorCachofeiro, Victoria-
dc.date.accessioned2022-10-11T10:27:12Z-
dc.date.available2022-10-11T10:27:12Z-
dc.date.issued2015-06-
dc.identifier.citationMiana M, Galán M, Martínez-Martínez E, Varona S, Jurado-López R, Bausa-Miranda B, Antequera A, Luaces M, Martínez-González J, Rodríguez C, Cachofeiro V. The lysyl oxidase inhibitor β-aminopropionitrile reduces body weight gain and improves the metabolic profile in diet-induced obesity in rats. Dis Model Mech. 2015 Jun;8(6):543-51. doi: 10.1242/dmm.020107. Epub 2015 Apr 7. PMID: 26035864; PMCID: PMC4457038.es_ES
dc.identifier.issn1754-8403-
dc.identifier.urihttps://hdl.handle.net/20.500.12530/56076-
dc.description.abstractExtracellular matrix (ECM) remodelling of the adipose tissue plays a pivotal role in the pathophysiology of obesity. The lysyl oxidase (LOX) family of amine oxidases, including LOX and LOX-like (LOXL) isoenzymes, controls ECM maturation, and upregulation of LOX activity is essential in fibrosis; however, its involvement in adipose tissue dysfunction in obesity is unclear. In this study, we observed that LOX is the main isoenzyme expressed in human adipose tissue and that its expression is strongly upregulated in samples from obese individuals that had been referred to bariatric surgery. LOX expression was also induced in the adipose tissue from male Wistar rats fed a high-fat diet (HFD). Interestingly, treatment with β-aminopropionitrile (BAPN), a specific and irreversible inhibitor of LOX activity, attenuated the increase in body weight and fat mass that was observed in obese animals and shifted adipocyte size toward smaller adipocytes. BAPN also ameliorated the increase in collagen content that was observed in adipose tissue from obese animals and improved several metabolic parameters - it ameliorated glucose and insulin levels, decreased homeostasis model assessment (HOMA) index and reduced plasma triglyceride levels. Furthermore, in white adipose tissue from obese animals, BAPN prevented the downregulation of adiponectin and glucose transporter 4 (GLUT4), as well as the increase in suppressor of cytokine signaling 3 (SOCS3) and dipeptidyl peptidase 4 (DPP4) levels, triggered by the HFD. Likewise, in the TNFα-induced insulin-resistant 3T3-L1 adipocyte model, BAPN prevented the downregulation of adiponectin and GLUT4 and the increase in SOCS3 levels, and consequently normalised insulin-stimulated glucose uptake. Therefore, our data provide evidence that LOX plays a pathologically relevant role in the metabolic dysfunction induced by obesity and emphasise the interest of novel pharmacological interventions that target adipose tissue fibrosis and LOX activity for the clinical management of this disease.es_ES
dc.description.sponsorshipPlan Estatal I+D+I 2013-2016 [PI12/01729, PI12/01952]. Red de Investigación Cardiovascular [RD12/0042/0033 and RD12/0042/0053], Instituto de Salud Carlos III (ISCIII). Ministerio de Economía y Competitividad (MINECO) [SAF2012-40127]. Fondo Europeo de Desarrollo Regional (FEDER). Sara Borrell Program, ISCIII (CD12/00589)es_ES
dc.language.isoenes_ES
dc.publisherThe Company of Biologistses_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectAdipose tissuees_ES
dc.subjectExtracellular matrixes_ES
dc.subjectFibrosises_ES
dc.subjectInsulin resistancees_ES
dc.subjectLysyl oxidasees_ES
dc.subjectObesityes_ES
dc.subject.mesh3T3-L1 Cellses_ES
dc.subject.meshAdipocyteses_ES
dc.subject.meshAdiponectines_ES
dc.subject.meshAdiposityes_ES
dc.subject.meshAminopropionitrilees_ES
dc.subject.meshAnimalses_ES
dc.subject.meshCell Sizees_ES
dc.subject.meshCollagenes_ES
dc.subject.meshDiet, High-Fates_ES
dc.subject.meshEnzyme Inhibitorses_ES
dc.subject.meshFemalees_ES
dc.subject.meshFibrosises_ES
dc.subject.meshGlucosees_ES
dc.subject.meshGlucose Transporter Type 4es_ES
dc.subject.meshHumanses_ES
dc.subject.meshInsulines_ES
dc.subject.meshInsulin Resistancees_ES
dc.subject.meshIntra-Abdominal Fates_ES
dc.subject.meshMalees_ES
dc.subject.meshMetabolomees_ES
dc.subject.meshMicees_ES
dc.subject.meshModels, Biologicales_ES
dc.subject.meshObesityes_ES
dc.subject.meshProtein-Lysine 6-Oxidasees_ES
dc.subject.meshRats, Wistares_ES
dc.subject.meshSignal Transductiones_ES
dc.subject.meshWeight Gaines_ES
dc.titleThe lysyl oxidase inhibitor β-aminopropionitrile reduces body weight gain and improves the metabolic profile in diet-induced obesity in ratses_ES
dc.typeArtículoes_ES
dc.identifier.pubmedID26035864es_ES
dc.format.volume8es_ES
dc.format.page543-551es_ES
dc.contributor.funderISCIIIes_ES
dc.contributor.funderMinisterio de Ciencia e Innovaciónes_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1242/dmm.020107es_ES
dc.identifier.journalDisease models & mechanismses_ES
dc.identifier.journalabbreviationDis Model Meches_ES
dc.contributor.authoraffiliationServicio de Cirugía. Hospital Universitario de Fuenlabradaes_ES
dc.format.number6es_ES
dc.subject.decsTejido Adiposoes_ES
dc.subject.decsAumento de Pesoes_ES
dc.subject.decsTransducción de Señales_ES
dc.subject.decsObesidades_ES
dc.subject.decsMetabolomaes_ES
dc.subject.decsResistencia a la Insulinaes_ES
dc.subject.decsGlucosaes_ES
Appears in Collections:Hospitales > H. U. de Fuenlabrada > Artículos

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