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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampVercesi, Anibal Eugenio-
dc.contributor.authorunicampOliveira, Helena Coutinho Franco de-
dc.typeArtigopt_BR
dc.titleMitochondrial energy metabolism and redox responses to hypertriglyceridemiapt_BR
dc.contributor.authorAlberici, Luciane C.-
dc.contributor.authorVercesi, Anibal E.-
dc.contributor.authorOliveira, Helena C. F.-
dc.subjectHipertrigliceridemiapt_BR
dc.subject.otherlanguageHypertriglyceridemiapt_BR
dc.description.abstractIn this work we review recent findings that explain how mitochondrial bioenergetic functions and redox state respond to a hyperlipidemic in vivo environment and may contribute to the maintenance of a normal metabolic phenotype. The experimental model utilized to evidence these adaptive mechanisms is especially useful for these studies since it exhibits genetic hypertriglyceridemia and avoids complications introduced by high fat diets. Liver from hypertrigliceridemic (HTG) mice have a greater content of glycerolipids together with increased mitochondrial free fatty acid oxidation. HTG liver mitochondria have a higher resting respiration rate but normal oxidative phosphorylation efficiency. This is achieved by higher activity of the mitochondrial potassium channel sensitive to ATP (mitoKATP). The mild uncoupling mediated by mitoKATP accelerates respiration rates and reduces reactive oxygen species generation. Although this response is not sufficient to inhibit lipid induced extra-mitochondrial oxidative stress in whole liver cells it avoids amplification of this redox imbalance. Furthermore, higher mitoKATP activity increases liver, brain and whole body metabolic rates. These mitochondrial adaptations may explain why these HTG mice do not develop insulin resistance and obesity even under a severe hyperlipidemic state. On the contrary, when long term high fat diets are employed, insulin resistance, fatty liver and obesity develop and mitochondrial adaptations are inefficient to counteract energy and redox imbalancespt_BR
dc.relation.ispartofJournal of bioenergetics and biomembranespt_BR
dc.relation.ispartofabbreviationJ. bioenerg. biomembr.pt_BR
dc.publisher.cityHeidelbergpt_BR
dc.publisher.countryAlemanhapt_BR
dc.publisherSpringerpt_BR
dc.date.issued2011-
dc.date.monthofcirculationFeb.pt_BR
dc.language.isoengpt_BR
dc.description.volume43pt_BR
dc.description.firstpage19pt_BR
dc.description.lastpage23pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0145-479Xpt_BR
dc.identifier.eissn1573-6881pt_BR
dc.identifier.doi10.1007/s10863-011-9326-ypt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs10863-011-9326-ypt_BR
dc.date.available2020-09-01T13:15:33Z-
dc.date.accessioned2020-09-01T13:15:33Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-09-01T13:15:33Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:48Z : No. of bitstreams: 1 000287970700004.pdf: 249916 bytes, checksum: 8234bc667354bd93cb4350ecb75236ab (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-01T13:15:33Z (GMT). No. of bitstreams: 0 Previous issue date: 2011en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348428-
dc.contributor.departmentDepartamento de Patologia Clínicapt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.subject.keywordMitochondrial uncouplingpt_BR
dc.subject.keywordRedox statept_BR
dc.subject.keywordMitochondrial ATP-sensitive potassium channelspt_BR
dc.identifier.source000287970700004pt_BR
dc.creator.orcid0000-0002-0504-5676pt_BR
dc.creator.orcid0000-0003-0119-6992pt_BR
dc.type.formArtigopt_BR
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