Regulation of adipose tissue metabolism in cancer cachexia.
OBJECTIVE
Body-fat depletion is a hallmark of cancer cachexia, a complex clinical syndrome associated with increased morbidity and mortality. Understanding the fat-loss disorder in cachexia is essential for the development of better treatments for the syndrome. This review presents recent studies focusing on the mechanisms of adipose atrophy in cancer cachexia, particularly the potential mediators.


RESULTS
Fat loss cannot be explained by poor appetite alone, and may also result from altered lipid metabolism in adipocytes. Increased lipolysis appears to be a key factor underlying fat loss in cancer cachexia though decreases in lipid deposition and adipocyte development may also contribute. Both tumour and host-derived factors are implicated in adipose tissue atrophy. Tumour necrosis factor-alpha has been associated with increased lipolysis in adipocytes. The novel adipokine zinc-alpha2-glycoprotein may function locally, as well as systemically, to promote lipid mobilization and utilization in cancer cachexia.


CONCLUSIONS
Clarifying the role of cachexia mediators in adipose tissue atrophy will add to our understanding of adipocyte metabolism in wasting disease. Elucidating their mode of action may lead to novel therapeutic targets for counteracting the cachexia syndrome.
Bing
Chen
C
Obesity Biology Unit, School of Clinical Sciences, University of Liverpool, Liverpool, UK. bing@liverpool.ac.uk
Trayhurn
Paul
P
D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D002100:Cachexia / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D050356:Lipid Metabolism; D008066:Lipolysis; D009369:Neoplasms / Q000378:metabolism*; D019282:Wasting Syndrome