期刊
SCIENCE
卷 333, 期 6039, 页码 233-238出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1198973
关键词
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资金
- Medical University of Graz
- Forschungsforderungsgesellschaft
- Bundesministerium fur Wissenschaft und Forschung
- SFB LIPOTOX [F30]
- Austrian Fonds zur Forderung der Wissenschaftlichen Forschung [Z136]
- Austrian Science Fund (FWF) [Z136] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [F 3008, Z 136, F 3002] Funding Source: researchfish
Cachexia is a multifactorial wasting syndrome most common in patients with cancer that is characterized by the uncontrolled loss of adipose and muscle mass. We show that the inhibition of lipolysis through genetic ablation of adipose triglyceride lipase (Atgl) or hormone-sensitive lipase (Hsl) ameliorates certain features of cancer-associated cachexia (CAC). In wild-type C57BL/6 mice, the injection of Lewis lung carcinoma or B16 melanoma cells causes tumor growth, loss of white adipose tissue (WAT), and a marked reduction of gastrocnemius muscle. In contrast, Atgl-deficient mice with tumors resisted increased WAT lipolysis, myocyte apoptosis, and proteasomal muscle degradation and maintained normal adipose and gastrocnemius muscle mass. Hsl-deficient mice with tumors were also protected although to a lesser degree. Thus, functional lipolysis is essential in the pathogenesis of CAC. Pharmacological inhibition of metabolic lipases may help prevent cachexia.
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