Adipose tissue lipolysis promotes exercise-induced cardiac hypertrophy involving the lipokine C16: 1n7-palmitoleate
Foryst-Ludwig A, Kreissl MC, Benz V, Brix S, Smeir E, Ban Z, Januszewicz E, Salatzki J, Grune J, Schwanstecher AK, Blumrich A, Schirbel A, Klopfleisch R, Rothe M, Blume K, Halle M, Wolfarth B, Kershaw EE, Kintscher U (2015)
Publication Type: Journal article
Publication year: 2015
Journal
Book Volume: 290
Pages Range: 23603-23615
Journal Issue: 39
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 accompaniedbythe absence of aplasma 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. Inconsonance, 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 alipokine involved in physiological cardiac growth may help to develop future lipid-based therapies for pathological LVH or heart failure.
Involved external institutions
Charité - Universitätsmedizin Berlin
Germany (DE)
Universitätsklinikum Würzburg
Germany (DE)
Freie Universität Berlin
Germany (DE)
Lipidomix GmbH
Germany (DE)
Technische Universität München (TUM)
Germany (DE)
University of Pittsburgh
United States (USA) (US)
Germany (DE)
Universitätsklinikum Würzburg
Germany (DE)
Freie Universität Berlin
Germany (DE)
Lipidomix GmbH
Germany (DE)
Technische Universität München (TUM)
Germany (DE)
University of Pittsburgh
United States (USA) (US)
How to cite
APA:
Foryst-Ludwig, A., Kreissl, M.C., Benz, V., Brix, S., Smeir, E., Ban, Z.,... Kintscher, U. (2015). Adipose tissue lipolysis promotes exercise-induced cardiac hypertrophy involving the lipokine C16: 1n7-palmitoleate. Journal of Biological Chemistry, 290(39), 23603-23615. https://doi.org/10.1074/jbc.M115.645341
MLA:
Foryst-Ludwig, Anna, et al. "Adipose tissue lipolysis promotes exercise-induced cardiac hypertrophy involving the lipokine C16: 1n7-palmitoleate." Journal of Biological Chemistry 290.39 (2015): 23603-23615.
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