Loss of body weight is a strong stimulus to food intake in humans. Therefore, the presence of CAC in patients with cancer suggests a failure of the adaptive feeding response. A large amount of evidence has been provided in the last few years on the regulation of feeding and body weight. Leptin, a recently found hormone produced by the adipocyte ob gene, has been shown to be an essential component of the homeostatic regulation of body weight. Leptin acts to control food intake and energy expenditure via a neuropeptidergic effect or molecules within the hypothalamus. Complex interactions take place among the nervous, endocrine and immune systems inducing behavioural and metabolic responses [38-44].
Proinflammatory cytokines, proposed as mediators of CAC, may have a central role in long-term inhibition of feeding by mimicking the hypothala-
mic effect of excessive negative feedback signalling from leptin. This could be via continuous stimulation of anorexigenic neuropeptides such as serotonin- and corticotropin-releasing factor, as well as by inhibition of the neuropeptide Y orexigenic network consisting of opioid peptides and galanin, and the recently identified melanin-concentrating hormone, orexin and agouti-related peptide. Such abnormalities in the hypothalamic neuropeptide loop in tumour-bearing animals lead to the development of CAC.
Although the present therapeutic use of neu-ropeptide agonists/antagonists is obesity treatment, this area could also be an effective target for the treatment of CAC, particularly in combination with other agents with different mechanisms of action [45,46].
A study by our group  demonstrated very low leptin levels associated with high levels of inflammatory cytokines in patients with advanced-stage cancer, several of whom had a significant body weight loss.
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