Cachexia: lessons from melanocortin antagonism

Mark D. DeBoer, Daniel L. Marks

Research output: Contribution to journalReview articlepeer-review

40 Scopus citations


It is well established that disruptions in melanocortin signaling in the CNS result in morbid obesity, but only recently has evidence linked the activation of this system with the production of cachexia, also known as disease-associated wasting. Pro-opiomelanocortin-producing neurons, which express cytokine receptors, show increased activation in the presence of several cytokines that are increased in diseases that are associated with cachexia. Recent experiments show that blockade of melanocortin signaling using antagonists to the melanocortin MC4 receptor attenuates disease-associated anorexia and wasting in rodent models of cancer and renal failure. This successful inhibition of cachexia is important because loss of appetite and lean body mass worsen the prognosis of many the diseases with which cachexia is associated.

Original languageEnglish (US)
Pages (from-to)199-204
Number of pages6
JournalTrends in Endocrinology and Metabolism
Issue number5
StatePublished - Jul 2006

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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