Central mechanisms controlling appetite and food intake in a cancer setting: an update.

Autumn L. Fletcher, Daniel Marks

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: Cachexia, also known as disease-associated wasting, is an important factor in the mortality of many patients with diseases such as cancer, as well as renal and congestive heart failure. Yet the syndrome is not yet well defined, making diagnosis difficult and often subjective on the part of the physician. Nor are the central mechanisms of cachexia fully elucidated. Recent studies have begun to address these gaps by focusing on three areas: the role of cytokines in cachexia, other proteins and peptides that might be involved, and potential treatments for this devastating syndrome. RECENT FINDINGS: Cachexia can be caused, in the absence of disease, by inflammatory stimuli and some chemotherapy drugs, suggesting possible central mechanisms in cachexia. Promising treatments include melanocortin antagonism and some hormones. SUMMARY: While more research is necessary to illuminate causal mechanisms and uncover potential therapies of cachexia, several of its major molecular pathways have become elucidated, suggesting directions for therapeutic approaches.

Original languageEnglish (US)
Pages (from-to)306-311
Number of pages6
JournalCurrent Opinion in Supportive and Palliative Care
Volume1
Issue number4
StatePublished - Dec 2007

Fingerprint

Cachexia
Appetite
Eating
Neoplasms
Melanocortins
Wasting Syndrome
Therapeutics
Heart Failure
Hormones
Cytokines
Physicians
Kidney
Drug Therapy
Peptides
Mortality
Research
Pharmaceutical Preparations
Proteins

ASJC Scopus subject areas

  • Oncology
  • Medicine(all)
  • Critical Care and Intensive Care Medicine
  • Oncology(nursing)

Cite this

Central mechanisms controlling appetite and food intake in a cancer setting : an update. / Fletcher, Autumn L.; Marks, Daniel.

In: Current Opinion in Supportive and Palliative Care, Vol. 1, No. 4, 12.2007, p. 306-311.

Research output: Contribution to journalArticle

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