Purpose of review: Anorexia is a severe debilitating symptom characterizing the clinical course of several chronic diseases. It negatively impacts on patient outcome by contributing to weight loss, lean body mass catabolism and adipose tissue wasting. Although disease-associated anorexia may stand alone as a clinically relevant symptom, it is now considered as a component of the cachexia syndrome. The present review discusses experimental and clinical data indicating that the pathogenic mechanisms of anorexia may also suggest a neural control of tissue wasting in cachexia.
Recent findings: Consistent data show that selective melanocortin receptor antagonism modulates food intake and reduces wasting in experimental models of chronic disease. Consequently, ghrelin administration, whose prophagic effects are related to melanocortin antagonism, has been tested both in animal studies and human trials, with promising effects, although restoration of lean body mass has been not achieved. More interest is driven by the use of small molecules selectively antagonising hypothalamic melanocortin receptors.
Summary: The 'brain-muscle axis' coordinated by the hypothalamus seems to mediate the onset of not only anorexia but also tissue wasting in cachexia, by centrally influencing energy homeostasis and the balance between anabolism and catabolism.