Adipose Triglyceride Lipase Contributes to Cancer-Associated Cachexia

Suman K. Das, Sandra Eder, Silvia Schauer, Clemens Diwoky, Hannes Temmel, Barbara Gürtl, Gregor Gorkiewicz, Kuppusamy P. Tamilarasan, Pooja Kumari, Michael Trauner, Robert Zimmermann, Paul Vesely, Günter Hämmerle, Rudolf Zechner*, Gerald Höfler*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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
Original languageEnglish
Pages (from-to)233-238
Issue number6039
Publication statusPublished - 2011

Fields of Expertise

  • Human- & Biotechnology

Treatment code (Nähere Zuordnung)

  • Basic - Fundamental (Grundlagenforschung)


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