Abstract
Implantation of a fast growing tumour to mice (Lewis lung carcinoma) resulted in a clear cachectic state characterized by a profound muscle wasting. This was accompanied by a significant increase in both UCP2 and UCP3 gene expression in skeletal muscle and heart. Interestingly, this increase in gene expression was not linked to a rise in circulating fatty acids or in a decrease in food intake, as previously reported in other pathophysiological states. These results question the concept that hyperlipaemia is the only factor controlling UCP gene expression in different pathophysiological conditions. In addition, the present work suggests that UCPs might participate in a counter-regulatory mechanism to lower the production of ROS.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Blotting, Northern
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Blotting, Western
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Cachexia / genetics
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Cachexia / metabolism*
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Cachexia / pathology
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Carrier Proteins / genetics*
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DNA Primers
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Disease Models, Animal
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Energy Intake*
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Fatty Acids / blood*
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Gene Expression Regulation*
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Ion Channels
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Membrane Transport Proteins / genetics*
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Mice
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Mice, Inbred C57BL
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Mitochondrial Proteins / genetics*
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Muscle, Skeletal / metabolism*
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Neoplasms, Experimental / genetics
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Neoplasms, Experimental / metabolism*
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Neoplasms, Experimental / pathology
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Reactive Oxygen Species*
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Reverse Transcriptase Polymerase Chain Reaction
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Uncoupling Protein 2
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Uncoupling Protein 3
Substances
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Carrier Proteins
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DNA Primers
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Fatty Acids
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Ion Channels
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Membrane Transport Proteins
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Mitochondrial Proteins
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Reactive Oxygen Species
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Ucp2 protein, mouse
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Ucp3 protein, mouse
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Uncoupling Protein 2
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Uncoupling Protein 3