Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/196968
Type: Artigo de periódico
Title: Hyperlipidemic Mice Present Enhanced Catabolism And Higher Mitochondrial Atp-sensitive K+ Channel Activity.
Author: Alberici, Luciane C
Oliveira, Helena C F
Patrício, Patrícia R
Kowaltowski, Alicia J
Vercesi, Anibal E
Abstract: 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. Oxidative metabolism and its response to mitochondrial adenosine triphosphate (ATP)-sensitive K+ channel (mitoK(ATP)) agonists and antagonists were measured in isolated mitochondria, livers, and mice. 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 mitoK(ATP) agonists and antagonists. Furthermore, mitochondrial binding to fluorescent glibenclamide indicates that HTG mice expressed higher quantities of mitoK(ATP). The higher content and activity of liver mitoK(ATP) resulted in a faster metabolic state, as evidenced by increased liver oxygen consumption and higher body CO(2) release and temperature in these mice. In agreement with higher metabolic rates, food ingestion was significantly larger in HTG mice, without enhanced weight gain. These results show that primary hyperlipidemia 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 mitoK(ATP), in addition to UCPs, may be involved in the control of energy metabolism and body weight.
Subject: Animals
Apolipoprotein C-iii
Body Temperature
Cell Respiration
Eating
Energy Metabolism
Fatty Acids
Humans
Hyperlipidemias
Metabolism
Mice
Mice, Transgenic
Mitochondria, Liver
Mitochondrial Swelling
Potassium Channels
Protein Structure, Tertiary
Rights: fechado
Identifier DOI: 10.1053/j.gastro.2006.07.021
Address: http://www.ncbi.nlm.nih.gov/pubmed/17030192
Date Issue: 2006
Appears in Collections:Unicamp - Artigos e Outros Documentos

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