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dc.contributor.authorFernandes, Joana L.
dc.contributor.authorMartins, Fátima O.
dc.contributor.authorOlea Fraile, Elena 
dc.contributor.authorPrieto Lloret, Jesús 
dc.contributor.authorBraga, Patrícia C.
dc.contributor.authorSacramento, Joana F.
dc.contributor.authorSequeira, Catarina O.
dc.contributor.authorNegrinho, Ana P.
dc.contributor.authorPereira, Sofia A.
dc.contributor.authorAlves, Marco G.
dc.contributor.authorRocher Martín, María Asunción 
dc.contributor.authorConde, Silvia V.
dc.date.accessioned2024-05-29T08:05:41Z
dc.date.available2024-05-29T08:05:41Z
dc.date.issued2023
dc.identifier.citationAntioxidants, 2023, Vol. 12, Nº. 11, 1910es
dc.identifier.issn2076-3921es
dc.identifier.urihttps://uvadoc.uva.es/handle/10324/67885
dc.descriptionProducción Científicaes
dc.description.abstractThe association between obstructive sleep apnea (OSA) and metabolic disorders is well-established; however, the underlying mechanisms that elucidate this relationship remain incompletely understood. Since the liver is a major organ in the maintenance of metabolic homeostasis, we hypothesize that liver dysfunction plays a crucial role in the pathogenesis of metabolic dysfunction associated with obstructive sleep apnea (OSA). Herein, we explored the underlying mechanisms of this association within the liver. Experiments were performed in male Wistar rats fed with a control or high fat (HF) diet (60% lipid-rich) for 12 weeks. Half of the groups were exposed to chronic intermittent hypoxia (CIH) (30 hypoxic (5% O2) cycles, 8 h/day) that mimics OSA, in the last 15 days. Insulin sensitivity and glucose tolerance were assessed. Liver samples were collected for evaluation of lipid deposition, insulin signaling, glucose homeostasis, hypoxia, oxidative stress, antioxidant defenses, mitochondrial biogenesis and inflammation. Both the CIH and HF diet induced dysmetabolism, a state not aggravated in animals submitted to HF plus CIH. CIH aggravates hepatic lipid deposition in obese animals. Hypoxia-inducible factors levels were altered by these stimuli. CIH decreased the levels of oxidative phosphorylation complexes in both groups and the levels of SOD-1. The HF diet reduced mitochondrial density and hepatic antioxidant capacity. The CIH and HF diet produced alterations in cysteine-related thiols and pro-inflammatory markers. The results obtained suggest that hepatic mitochondrial dysfunction and oxidative stress, leading to inflammation, may be significant factors contributing to the development of dysmetabolism associated with OSA.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherMDPIes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectSleep disorderses
dc.subjectObstructive sleep apneanes
dc.subjectChronic intermittent hypoxiaes
dc.subjectInsulin resistancees
dc.subjectMetabolic disorderses
dc.subjectMitochondrial dysfunctiones
dc.subjectInflammationes
dc.titleChronic intermittent hypoxia-induced dysmetabolism is associated with hepatic oxidative stress, mitochondrial dysfunction and inflammationes
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2023 The authorses
dc.identifier.doi10.3390/antiox12111910es
dc.relation.publisherversionhttps://www.mdpi.com/2076-3921/12/11/1910es
dc.identifier.publicationfirstpage1910es
dc.identifier.publicationissue11es
dc.identifier.publicationtitleAntioxidantses
dc.identifier.publicationvolume12es
dc.peerreviewedSIes
dc.description.projectJunta de Castilla y León y Sociedad Portugal de Diabetes (Grupo de Investigaión Fundamental e Translacional) - (grant CCVC8485)es
dc.description.projectFundación Portuguesa para la Ciencia y la Tecnología (FCT) - (CEECIND/04266/2017, CEEC IND/02428/2018 y 2021.03439.CEECIND)es
dc.description.projectFundación Portuguesa para la Ciencia y la Tecnología (FCT) - (projects UIDB/04050/2020 and UIDB/04033/2020)es
dc.description.projectLaboratorio de Investigación Integrativa y Traslacional en Salud de la Población (ITR) (LA/P/0064/2020) - (project UI/BD/150750/2020)es
dc.identifier.essn2076-3921es
dc.rightsAtribución 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones
dc.subject.unesco32 Ciencias Médicases
dc.subject.unesco2411.08 Metabolismo Humanoes
dc.subject.unesco2415 Biología Moleculares
dc.subject.unesco2302 Bioquímicaes


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