Hyperlipidemic mice present enhanced catabolism and higher mitochondrial ATP-sensitive K+ channel activity

dc.creatorAlberici, LC
dc.creatorOliveira, HCF
dc.creatorPatricio, PR
dc.creatorKowaltowski, AJ
dc.creatorVercesi, AE
dc.date2006
dc.dateOCT
dc.date2014-11-14T05:42:20Z
dc.date2015-11-26T16:04:42Z
dc.date2014-11-14T05:42:20Z
dc.date2015-11-26T16:04:42Z
dc.date.accessioned2018-03-28T22:53:48Z
dc.date.available2018-03-28T22:53:48Z
dc.identifierGastroenterology. W B Saunders Co-elsevier Inc, v. 131, n. 4, n. 1228, n. 1234, 2006.
dc.identifier0016-5085
dc.identifierWOS:000241246800032
dc.identifier10.1053/j.gastro.2006.07.021
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/69062
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/69062
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/69062
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1265552
dc.descriptionBackground & Aims: Changes in mitochondrial energy metabolism promoted by uncoupling proteins (UCPs) are often found in metabolic disorders. We have recently shown that hypertriglyceridemic (HTG) mice present higher mitochondrial resting respiration unrelated to UCPs. Here, we disclose the underlying mechanism and consequences, in tissue and whole body metabolism, of this mitochondrial response to hyperlipidemia. Methods: Oxidative metabolism and its response to mitochondrial adenosine rriphosphate (ATP)-sensitive K+ channel (mitoK(ATP)) agonists and antagonists were measured in isolated mitochondria, livers, and mice. Results: Mitochondria isolated from the livers of HTG mice presented enhanced respiratory rates compared with those from wild-type mice. Changes in oxygen consumption were sensitive to adenosine triphosphate (ATP), diazoxide, and 5-hydroxydecanoate, indicating they are attributable to mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) activity. Indeed, mitochondria from HTG mice presented enhanced swelling in the presence of K+ ions, sensitive to mitoKATpagonists and antagonists. Furthermore, mitochondrial binding to fluorescent glibenclamide indicates that HTG mice expressed higher quantities of mitoKATp. The higher content and activity of liver mitoKATpresulted in a faster metabolic state, as evidenced by increased liver oxygen consumption and higher body CO2 release and temperature in these mice. In agreement with higher metabolic rates, food ingestion was significantly larger in HTG mice, without enhanced weight gain. Conclusions: These results show that primary hyperlipidernia leads to an elevation in liver mitoK(ATp)activity, which may represent a regulated adaptation to oxidize excess fatty acids in HTG mice. Furthermore, our data indicate that mitoKATP, in addition to UCPs, may be involved in the control of energy metabolism and body weight.
dc.description131
dc.description4
dc.description1228
dc.description1234
dc.languageen
dc.publisherW B Saunders Co-elsevier Inc
dc.publisherPhiladelphia
dc.publisherEUA
dc.relationGastroenterology
dc.relationGastroenterology
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectUncoupling Protein-3
dc.subjectSkeletal-muscle
dc.subjectTransgenic Mice
dc.subjectInsulin-resistance
dc.subjectPotassium Channel
dc.subjectGene-expression
dc.subjectHypertriglyceridemic Mice
dc.subjectThyroid-hormone
dc.subjectIii Gene
dc.subjectApo-ciii
dc.titleHyperlipidemic mice present enhanced catabolism and higher mitochondrial ATP-sensitive K+ channel activity
dc.typeArtículos de revistas


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