Abstract
Skeletal muscle is a tissue of high demand and it accounts for most of daily energy consumption. The classical concept of energy metabolism in skeletal muscle has been profoundly modified on the basis of studies showing the influence of additional factors (i.e., uncoupling proteins (UCPs) and peroxisome proliferator activated receptors (PPARs)) controlling parameters, such as substrate availability, cellular enzymes, carrier proteins, and proton leak, able to affect glycolysis, nutrient oxidation, and protein degradation. This extremely balanced system is greatly altered by cancer disease that can induce muscle cachexia with significant deleterious consequences and results in muscle wasting and weakness, delaying or preventing ambulation, and rehabilitation in catabolic patients.
Copyright 2003 Wiley-Liss, Inc.
MeSH terms
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Animals
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Cachexia / metabolism
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Carrier Proteins / metabolism
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Cysteine Endopeptidases / metabolism
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Cytokines / metabolism
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Glucose / metabolism
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Humans
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Ion Channels
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Lipid Metabolism
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Lipoproteins, LDL / metabolism
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Membrane Proteins / metabolism
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Mitochondria / metabolism
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Mitochondrial Proteins
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Multienzyme Complexes / metabolism
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Muscle, Skeletal / cytology
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Muscle, Skeletal / metabolism*
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Muscle, Skeletal / physiology*
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Neoplasms / metabolism*
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Proteasome Endopeptidase Complex
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Receptors, Cytoplasmic and Nuclear / metabolism
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Receptors, Retinoic Acid / metabolism
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Retinoid X Receptors
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Transcription Factors / metabolism
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Triglycerides / metabolism
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Uncoupling Agents / metabolism
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Uncoupling Protein 1
Substances
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Carrier Proteins
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Cytokines
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Ion Channels
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Lipoproteins, LDL
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Membrane Proteins
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Mitochondrial Proteins
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Multienzyme Complexes
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Receptors, Cytoplasmic and Nuclear
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Receptors, Retinoic Acid
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Retinoid X Receptors
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Transcription Factors
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Triglycerides
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Uncoupling Agents
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Uncoupling Protein 1
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Cysteine Endopeptidases
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Proteasome Endopeptidase Complex
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Glucose