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

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F16%3A00466490" target="_blank" >RIV/67985823:_____/16:00466490 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1038/nm.4171" target="_blank" >http://dx.doi.org/10.1038/nm.4171</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/nm.4171" target="_blank" >10.1038/nm.4171</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

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

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FB - Endocrinology, diabetology, metabolism, nutrition

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/7E12073" target="_blank" >7E12073: DIABAT - Recruitment and activation of brown adipocytes as preventive and curative therapy for type 2 diabetes</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Nature Medicine

  • ISSN

    1078-8956

  • e-ISSN

  • Volume of the periodical

    22

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    11

  • Pages from-to

    1120-1130

  • UT code for WoS article

    000384872500015

  • EID of the result in the Scopus database

    2-s2.0-84984622665