dc.creatorAlberici, Luciane C
dc.creatorOliveira, Helena C F
dc.creatorBighetti, Eliete J B
dc.creatorde Faria, Eliana C
dc.creatorDegaspari, Giovana R
dc.creatorSouza, Claudio T
dc.creatorVercesi, Anibal E
dc.date2003-Oct
dc.date2015-11-27T12:52:39Z
dc.date2015-11-27T12:52:39Z
dc.date.accessioned2018-03-29T00:58:26Z
dc.date.available2018-03-29T00:58:26Z
dc.identifierJournal Of Bioenergetics And Biomembranes. v. 35, n. 5, p. 451-7, 2003-Oct.
dc.identifier0145-479X
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/14740893
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195642
dc.identifier14740893
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1295875
dc.descriptionHigh plasma level of triglycerides (TGs) is a common feature in atherosclerosis, obesity, diabetes, alcoholism, stress, and infection. Since mitochondria have been implicated in cell death under a variety of metabolic disorders, we examined liver mitochondrial functions in hypertriglyceridemic transgenic mice. Hypertriglyceridemia increased resting respiration and predisposed to mitochondrial permeability transition (MPT). Ciprofibrate therapy reduced plasma TG levels, normalized respiration, and prevented MPT. The higher resting respiration in transgenic mitochondria remained in the presence of the adenine nucleotide carrier inhibitor, carboxyatractyloside, bovine serum albumin, and the uncoupling proteins (UCPs) inhibitor, GDP. UCP2 content was similar in both control and transgenic mitochondria. We propose that faster resting respiration represents a regulated adaptation to oxidize excess free fatty acid in the transgenic mice.
dc.description35
dc.description451-7
dc.languageeng
dc.relationJournal Of Bioenergetics And Biomembranes
dc.relationJ. Bioenerg. Biomembr.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAnimals
dc.subjectAtractyloside
dc.subjectCell Respiration
dc.subjectClofibric Acid
dc.subjectFibric Acids
dc.subjectGuanosine Diphosphate
dc.subjectHypertriglyceridemia
dc.subjectHypolipidemic Agents
dc.subjectIon Channels
dc.subjectLiver
dc.subjectMembrane Potentials
dc.subjectMembrane Transport Proteins
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectMitochondria
dc.subjectMitochondrial Proteins
dc.subjectSerum Albumin, Bovine
dc.subjectTriglycerides
dc.titleHypertriglyceridemia Increases Mitochondrial Resting Respiration And Susceptibility To Permeability Transition.
dc.typeArtículos de revistas


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