Fachbereich Veterinärmedizin



    Adipose Tissue Lipolysis Promotes Exercise-induced Cardiac Hypertrophy Involving the Lipokine C16:1n7-Palmitoleate (2015)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Foryst-Ludwig, Anna
    Kreissl, Michael C
    Benz, Verena
    Brix, Sarah
    Smeir, Elia
    Ban, Zsofia
    Januszewicz, Elżbieta
    Salatzki, Janek
    Grune, Jana
    Schwanstecher, Anne-Kathrin
    Blumrich, Annelie
    Schirbel, Andreas
    Klopfleisch, Robert (WE 12)
    Rothe, Michael
    Blume, Katharina
    Halle, Martin
    Wolfarth, Bernd
    Kershaw, Erin E
    Kintscher, Ulrich
    The journal of biological chemistry; 290(39) — S. 23603–23615
    ISSN: 0021-9258
    DOI: 10.1074/jbc.M115.645341
    Pubmed: 26260790
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
    +49 30 838 62450

    Abstract / Zusammenfassung

    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.