Evidence map›Paper›PMID 27571348›Full record

ArticleNature medicine2016

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

Maria Rohm, Michaela Schäfer, Victor Laurent, Bilgen Ekim Üstünel, Katharina Niopek, Carolyn Algire, Oksana Hautzinger, Tjeerd P Sijmonsma, Annika Zota, Dasa Medrikova and 16 more

Abstract read
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In one paragraph

Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
8.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

101 citing papers in PubMed, 148 citations in OpenAlex.

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  13. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review
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  17. Article
  18. Article
  19. Article
  20. Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025
    Review

41 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors at 8 institutions in 7 countries.

Maria RohmInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Michaela SchäferInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Victor LaurentInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Bilgen Ekim ÜstünelInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Katharina NiopekInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Carolyn AlgireInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Oksana HautzingerInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Tjeerd P SijmonsmaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Annika ZotaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Dasa MedrikovaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Natalia S PellegataInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Mikael RydenLipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
Agné KulyteLipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
Ingrid DahlmanLipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
Peter ArnerLipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
Natasa PetrovicDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Barbara CannonDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Ez-Zoubir AmriUniversité Côte d'Azur, Nice, France.ORCID 0000-0001-8426-5396
Bruce E KempSt Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria, Australia.
Gregory R SteinbergDepartment of Medicine, Division of Endocrinology and Metabolism, McMaster University, Hamilton, Ontario, Canada.
Petra JanovskaDepartment of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Jan KopeckyDepartment of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Christian WolfrumSwiss Federal Institute of Technology, Institute of Food Nutrition and Health, Schwerzenbach, Switzerland.
Matthias BlüherDepartment of Medicine, University of Leipzig, Leipzig, Germany.
Mauricio Berriel DiazInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Stephan HerzigInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Heidelberg University · DEKarolinska Institutet · SECzech Academy of Sciences · CZStockholm University · SECentre National de la Recherche Scientifique · FRLeipzig University · DEMcMaster University · CAThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Adipocytes, WhiteAdipose Tissue, WhiteAMP-Activated Protein KinasesAnimalsApoptosis Regulatory ProteinsCachexiaCells, CulturedIn Vitro TechniquesLipid MetabolismLipogenesisLipolysisMiceNeoplasmsPeptide FragmentsThermogenesisUncoupling Protein 1AMP-Activated Protein KinasesApoptosis Regulatory ProteinsCidea protein, mousePeptide FragmentsPrkab1 protein, mouseUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID27571348
OpenAlexW2509370928

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.