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Cancer cachexia

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Cachexia is the wasting of muscle that cannot be reversed by nutrition and is normally associated with a poor prognosis.  This is commonly seen in those patients with cancer, along with a number of other conditions.  This weakens the patients, opening them up to number of complications and reducing the likelihood of them responding to treatment. 


Leptin is a protein that is secreted by adipocytes and acts in the central nervous system, particularly in the hypothalamus, to suppress appetite and increase energy expenditure.  Leptin levels are low in gastrointestinal and pancreatic cancers, but are conversely high in breast cancers.


Ghrelin is a peptide hormone and stimulates the release of growth hormone, meaning that it regulates energy homeostasis.  Ghrelin infusions in cachectic patients has been shown to increase appetite and weight, hence reducing the effects of the unintended weight loss.
Adiponectin is another important factor in this area.  During adipocyte differentiation, adiponectin is produced in response to insulin and insulin-like growth factor.  High adiponectin levels have been associated with low weight but, as yet, levels have not been established with cancer induced cachexia.


Impaired response of leptin, ghrelin and adiponectin may be involved in the pathogenesis of cancer cachexia, especially in breast and colon cancer.  In response to weight loss, ghrelin and adiponectin levels increase while leptin levels decrease.


This information then begs the question, could pharmacological treatments enhance or inhibit the action of these substances to increase the quality of life and prognosis for these patients?  It must be understood than cancer cachexia is an extremely complex process involving many pathways and second messengers but if the correct ones can be intervened and reverted back to normal, this would surely redress the imbalance.


If a leptin infusion were to be given, would the hypothalamus be sensitive to the increased levels to exert the desired response?  If there were a way to inhibit the effects of insulin, maybe by using a low sugar diet, or chemically blocking the release of adiponectin then would the cachectic effects be reduced?  And similarly, if there were a way to temporarily interfere with ghrelin levels, would this also exert visible benefits?  Would interruption of one of these mediators be enough, or would all 3 need to be changed in order to improve prognosis?  Only time, and more research, will tell!


 

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