Evidence map›Paper›PMID 26260790›Full record

ArticleThe Journal of biological chemistry2015

Adipose Tissue Lipolysis Promotes Exercise-induced Cardiac Hypertrophy Involving the Lipokine C16:1n7-Palmitoleate.

Anna Foryst-Ludwig, Michael C Kreissl, Verena Benz, Sarah Brix, Elia Smeir, Zsofia Ban, Elżbieta Januszewicz, Janek Salatzki, Jana Grune, Anne-Kathrin Schwanstecher and 9 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 66 citations in OpenAlex.

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  19. Exercise training in heart transplantation.World journal of transplantation · 2021
    Review
  20. Proteomic Analysis ofPathogens (Basel, Switzerland) · 2021
    Article
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

19 authors at 6 institutions in 2 countries.

Anna Foryst-LudwigFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany, the DZHK (German Center for Cardiovascular Research), 10115 Berlin, Germany.
Michael C Kreisslthe Department of Nuclear Medicine, University Hospital Wuerzburg, 97080 Wuerzburg, Germany.
Verena BenzFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Sarah BrixFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Elia SmeirFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Zsofia BanFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Elżbieta JanuszewiczFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Janek SalatzkiFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Jana GruneFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Anne-Kathrin SchwanstecherFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Annelie BlumrichFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Andreas Schirbelthe Department of Nuclear Medicine, University Hospital Wuerzburg, 97080 Wuerzburg, Germany.
Robert Klopfleischthe Department of Veterinary Pathology, College of Veterinary Medicine, Freie Universität Berlin, 14163 Berlin, Germany.
Michael Rothethe Lipidomix GmbH, 13088 Berlin, Germany.
Katharina Blumethe Department of Prevention, Rehabilitation, and Sports Medicine, Technische Universitaet Muenchen, 80809 Muenchen, Germany.
Martin Hallethe Department of Prevention, Rehabilitation, and Sports Medicine, Technische Universitaet Muenchen, 80809 Muenchen, Germany, the DZHK (German Center for Cardiovascular Research), Munich Heart Alliance, 80809 Munich, Germany.
Bernd Wolfarththe Department of Sports Medicine, Humboldt University/Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany.
Erin E Kershawthe Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, and.
Ulrich KintscherFrom the Institute of Pharmacology, Center for Cardiovascular Research, Charité-Universitaetsmedizin Berlin, 10115 Berlin, Germany, the DZHK (German Center for Cardiovascular Research), 10115 Berlin, Germany ulrich.kintscher@charite.de.
Charité - Universitätsmedizin Berlin · DEGerman Centre for Cardiovascular Research · DEUniversitätsklinikum Würzburg · DEFreie Universität Berlin · DELipidomix (Germany) · DEUniversity of Pittsburgh · US

Funding

Adipose Triglyceride Lipase (ATGL) in Lipotoxicity and The Metabolic SyndromeR01DK090166 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KERSHAW, ERIN E. · 2011 to 2015
$1.7M
Howard Hughes Medical InstituteNIDDK NIH HHS R01 DK090166NIDDK NIH HHS R01DK090166
6 · The paper itself

Abstract

Endurance exercise training induces substantial adaptive cardiac modifications such as left ventricular hypertrophy (LVH). Simultaneously to the development of LVH, adipose tissue (AT) lipolysis becomes elevated upon endurance training to cope with enhanced energy demands. In this study, we investigated the impact of adipose tissue lipolysis on the development of exercise-induced cardiac hypertrophy. Mice deficient for adipose triglyceride lipase (Atgl) in AT (atATGL-KO) were challenged with chronic treadmill running. Exercise-induced AT lipolytic activity was significantly reduced in atATGL-KO mice accompanied by the absence of a plasma fatty acid (FA) increase. These processes were directly associated with a prominent attenuation of myocardial FA uptake in atATGL-KO and a significant reduction of the cardiac hypertrophic response to exercise. FA serum profiling revealed palmitoleic acid (C16:1n7) as a new molecular co-mediator of exercise-induced cardiac hypertrophy by inducing nonproliferative cardiomyocyte growth. In parallel, serum FA analysis and echocardiography were performed in 25 endurance athletes. In consonance, the serum C16:1n7 palmitoleate level exhibited a significantly positive correlation with diastolic interventricular septum thickness in those athletes. No correlation existed between linoleic acid (18:2n6) and diastolic interventricular septum thickness. Collectively, our data provide the first evidence that adipose tissue lipolysis directly promotes the development of exercise-induced cardiac hypertrophy involving the lipokine C16:1n7 palmitoleate as a molecular co-mediator. The identification of a lipokine involved in physiological cardiac growth may help to develop future lipid-based therapies for pathological LVH or heart failure.

Indexed as

LipolysisPhysical Conditioning, AnimalAdipose TissueAnimalsCardiomegalyCell LineFatty Acids, MonounsaturatedMiceMice, KnockoutFatty Acids, Monounsaturatedpalmitoleic acidadipose tissue metabolismadipose triglyceride lipase (ATGL)cardiac hypertrophycardiac metabolismlipid signaling

Identifiers

PMID26260790
PMCPMC4583014
OpenAlexW1137470125

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.