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Cancer cachexia

Tisdale, Michael J

Current Opinion in Gastroenterology: March 2010 - Volume 26 - Issue 2 - p 146–151
doi: 10.1097/MOG.0b013e3283347e77
Nutrition: Edited by David H. Alpers and William F. Stenson
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Purpose of review Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area.

Recent findings Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the α-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia.

Summary These findings provide impetus for the development of new therapeutic agents.

Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham, UK

Correspondence to Michael J. Tisdale, Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham B4 7ET, UK Tel: +44 121 204 4021; fax: +44 121 204 3743; e-mail: m.j.tisdale@aston.ac.uk

© 2010 Lippincott Williams & Wilkins, Inc.