Abstract
This study deals with mitochondrial energy efficiency in liver and skeletal muscle mitochondria in 15 days cold exposed rats. Cold exposure strongly increases the sensitivity to uncoupling by added palmitate of skeletal muscle but not liver mitochondria, while mitochondrial energy coupling in the absence of fatty acids is only slightly affected by cold in liver and skeletal muscle. In addition, uncoupling protein 3 content does not follow changes in skeletal muscle mitochondrial coupling. It is therefore concluded that skeletal muscle could play a direct thermogenic role based on fatty acid-induced mild uncoupling of mitochondrial oxidative phosphorylation.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Body Temperature Regulation / drug effects
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Body Temperature Regulation / physiology*
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Carrier Proteins / analysis
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Carrier Proteins / metabolism
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Cold Temperature*
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Electron Transport Complex IV / analysis
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Electron Transport Complex IV / metabolism
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Ion Channels
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Liver / drug effects
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Liver / enzymology
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Liver / metabolism
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Male
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Mitochondria, Liver / metabolism*
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Mitochondria, Muscle / metabolism*
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Mitochondrial ADP, ATP Translocases / analysis
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Mitochondrial ADP, ATP Translocases / metabolism
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Mitochondrial Proteins
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Muscle, Skeletal / drug effects
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Muscle, Skeletal / enzymology
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Muscle, Skeletal / metabolism
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Oxidative Phosphorylation / drug effects
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Oxygen Consumption
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Palmitates / pharmacology
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Rats
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Rats, Wistar
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Uncoupling Agents / pharmacology
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Uncoupling Protein 3
Substances
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Carrier Proteins
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Ion Channels
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Mitochondrial Proteins
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Palmitates
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Ucp3 protein, rat
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Uncoupling Agents
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Uncoupling Protein 3
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Mitochondrial ADP, ATP Translocases
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Electron Transport Complex IV