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  • Rohm, Maria (author)

An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice

  • Article/chapterEnglish2016

Publisher, publication year, extent ...

  • 2016-08-29
  • Springer Science and Business Media LLC,2016
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:su-136107
  • https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-136107URI
  • https://doi.org/10.1038/nm.4171DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:134371900URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • 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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Added entries (persons, corporate bodies, meetings, titles ...)

  • Schäfer, Michaela (author)
  • Laurent, Victor (author)
  • Üstünel, Bilgen Ekim (author)
  • Niopek, Katharina (author)
  • Algire, Carolyn (author)
  • Hautzinger, Oksana (author)
  • Sijmonsma, Tjeerd P. (author)
  • Zota, Annika (author)
  • Medrikova, Dasa (author)
  • Pellegata, Natalia S. (author)
  • Ryden, MikaelKarolinska Institutet (author)
  • Kulyte, AgnéKarolinska Institutet (author)
  • Dahlman, IngridKarolinska Institutet (author)
  • Arner, PeterKarolinska Institutet (author)
  • Petrovic, NatasaStockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut(Swepub:su)npetr (author)
  • Cannon, BarbaraStockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut(Swepub:su)canno (author)
  • Amri, Ez-Zoubir (author)
  • Kemp, Bruce E. (author)
  • Steinberg, Gregory R. (author)
  • Janovska, Petra (author)
  • Kopecky, Jan (author)
  • Wolfrum, Christian (author)
  • Blüher, Matthias (author)
  • Diaz, Mauricio Berriel (author)
  • Herzig, Stephan (author)
  • Karolinska InstitutetInstitutionen för molekylär biovetenskap, Wenner-Grens institut (creator_code:org_t)

Related titles

  • In:Nature Medicine: Springer Science and Business Media LLC22:10, s. 1120-11301078-89561546-170X

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