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Type: Artigo
Title: Mitochondrial energy metabolism and redox responses to hypertriglyceridemia
Author: Alberici, Luciane C.
Vercesi, Anibal E.
Oliveira, Helena C. F.
Abstract: In 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 imbalances
Subject: Hipertrigliceridemia
Country: Alemanha
Editor: Springer
Rights: Fechado
Identifier DOI: 10.1007/s10863-011-9326-y
Date Issue: 2011
Appears in Collections:IB - Artigos e Outros Documentos
FCM - Artigos e Outros Documentos

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