Publikationsdatenbank

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

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

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

Quelle

The journal of biological chemistry

Bandzählung: 290

Heftzählung: 39

Seiten: 23603 – 23615

ISSN: 0021-9258

Sprache

Englisch

Verweise

DOI: 10.1074/jbc.M115.645341

Pubmed: 26260790

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

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.