Hypercatabolism and hypermetabolism in wasting states.
The year 2001/2002 has been marked by a number of exciting new results for our understanding of anabolic and catabolic mediators and their participation in wasting states, as reflected by the contents of this section. It becomes ever more apparent that a clear understanding of how to shut off hypercatabolic and hypermetabolic processes is needed to underpin effective strategies for wasting syndromes. A particularly interesting development in the control of degradative processes in skeletal muscle is the discovery of several muscle-specific ubiquitin ligases. These enzymes, which confer specificity to the degradation of myofibrillar proteins and are situated in a pathway of proteolysis common to a variety of wasting states, may prove to be a valuable point of intervention in muscle atrophy. In the clinical arena, studies on non-small cell lung cancer patients as well as broader patient populations with solid tumours provide more evidence for a high incidence of hypermetabolism as well as low energy intake. The best therapies currently available for the cancer cachexia/anorexia syndrome have numerous limitations and tend mainly to attenuate losses rather than to promote a net gain of weight or lean body mass. Sustained hypermetabolism over the long course of disease progression constitutes an important contributor to negative energy balance, and its presence is likely to be a limiting factor to the success of current treatment approaches.
Baracos
Vickie E
VE
D000855:Anorexia / Q000378:metabolism / Q000628:therapy; D002100:Cachexia / Q000378:metabolism / Q000628:therapy; D004734:Energy Metabolism; D006801:Humans; D008025:Ligases / Q000378:metabolism*; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000201:enzymology*; D009133:Muscular Atrophy / Q000517:prevention & control; D044767:Ubiquitin-Protein Ligases; D019282:Wasting Syndrome / Q000378:metabolism*
D009124:Muscle Proteins; D044767:Ubiquitin-Protein Ligases; D008025:Ligases