Skeletal muscle metabolism in physiology and in cancer disease
- 18 August 2003
- journal article
- review article
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 90 (1) , 170-186
- https://doi.org/10.1002/jcb.10601
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. J. Cell. Biochem. 90: 170–186, 2003.Keywords
This publication has 103 references indexed in Scilit:
- Cachexia in cancer patientsNature Reviews Cancer, 2002
- Expression of Genes Involved in Lipid Metabolism Correlate with Peroxisome Proliferator-Activated Receptor Expression in Human Skeletal MuscleJournal of Clinical Endocrinology & Metabolism, 2000
- Peroxisome proliferator–activated receptor α mediates the adaptive response to fastingJournal of Clinical Investigation, 1999
- Genomic Organization and Regulation by Dietary Fat of the Uncoupling Protein 3 and 2 GenesBiochemical and Biophysical Research Communications, 1999
- In the rat, tumor necrosis factor α administration results in an increase in both UCP2 and UCP3 mRNAs in skeletal muscle: a possible mechanism for cytokine‐induced thermogenesis?FEBS Letters, 1998
- A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator- activated receptor alpha- deficient mice.Journal of Clinical Investigation, 1998
- Growth hormone, insulin, and somatostatin therapy of cancer cachexiaCancer, 1994
- Thermogenesis in Brown Adipose Tissue as an Energy BufferNew England Journal of Medicine, 1984
- Stimulation of Muscle Protein Degradation and Prostaglandin E2Release by Leukocytic Pyrogen (Interleukin-1)New England Journal of Medicine, 1983
- Whole Body Protein Synthesis and Turnover in Normal Man and Malnourished Patients with and without Known CancerAnnals of Surgery, 1981