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Rohm, Maria; Schäfer, Michaela; Laurent, Victor; Üstünel, Bilgen Ekim; Niopek, Katharina; Algire, Carolyn; Hautzinger, Oksana; Sijmonsma, Tjeerd P; Zota, Annika; Medrikova, Dasa; Pellegata, Natalia S; Ryden, Mikael; Kulyte, Agné; Dahlman, Ingrid; Arner, Peter; Petrovic, Natasa; Cannon, Barbara; Amri, Ez-Zoubir; Kemp, Bruce E; Steinberg, Gregory R; Janovska, Petra; Kopecky, Jan; Wolfrum, Christian; Blüher, Matthias; Berriel Diaz, Mauricio; Herzig, Stephan
Nature medicine, 10/2016, Letnik: 22, Številka: 10Journal Article
Cachexia represents a fatal energy-wasting syndrome in a large number of patients with cancer that mostly results in a pathological loss of skeletal muscle and adipose tissue. Here we show that tumor cell exposure and tumor growth in mice triggered a futile energy-wasting cycle in cultured white adipocytes and white adipose tissue (WAT), respectively. Although uncoupling protein 1 (Ucp1)-dependent thermogenesis was dispensable for tumor-induced body wasting, WAT from cachectic mice and tumor-cell-supernatant-treated adipocytes were consistently characterized by the simultaneous induction of both lipolytic and lipogenic pathways. Paradoxically, this was accompanied by an inactivated AMP-activated protein kinase (Ampk), which is normally activated in peripheral tissues during states of low cellular energy. Ampk inactivation correlated with its degradation and with upregulation of the Ampk-interacting protein Cidea. Therefore, we developed an Ampk-stabilizing peptide, ACIP, which was able to ameliorate WAT wasting in vitro and in vivo by shielding the Cidea-targeted interaction surface on Ampk. Thus, our data establish the Ucp1-independent remodeling of adipocyte lipid homeostasis as a key event in tumor-induced WAT wasting, and we propose the ACIP-dependent preservation of Ampk integrity in the WAT as a concept in future therapies for cachexia.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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