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Wednesday, 11 November 2015

Perfekt reguliert

Fluoreszenzmarkiertes G0S2 (grün) auf der Oberfläche von gespeicherten Lipidtröpfchen (rot) in einer kultivierten Herzzelle, aufgenommen mit einem konfokalen Fluoreszenzmikroskop. Foto: Uni Graz/IMB

Fluoreszenzmarkiertes G0S2 (grün) auf der Oberfläche von gespeicherten Lipidtröpfchen (rot) in einer kultivierten Herzzelle, aufgenommen mit einem konfokalen Fluoreszenzmikroskop. Foto: Uni Graz/IMB

ForscherInnen der Uni Graz zeigen Rolle des Proteins G0S2 für den Fettabbau im Herzen auf

Störungen in der Regulation des Fettstoffwechsels im Herzen sind Ursache für verschiedene Erkrankungen, wie etwa eine Herzmuskelschwäche im Zusammenhang mit Diabetes. Gesteuert werden die biochemischen Prozesse in unserem Körper unter anderem von verschiedensten Proteinen und Enzymen. ForscherInnen der Arbeitsgruppe um Univ.-Prof. Dr. Rudolf Zechner am Institut für Molekulare Biowissenschaften der Karl-Franzens-Universität Graz konnten nun die hemmende Wirkung des Proteins G0S2 auf den Fettabbau im Herzen belegen. Die Ergebnisse ihrer Arbeit wurden kürzlich im renommierten Journal of Biological Chemistry publiziert.

Die Konzentration des Proteins G0S2, das den Fettstoffwechsel reguliert, ist stark von der Nahrungsaufnahme abhängig. Doch diese Wechselwirkung funktioniert nicht in allen Körperzellen gleich. ForscherInnen der Uni Graz haben jetzt erstmals den Zusammenhang zwischen Nahrungsaufnahme, G0S2-Spiegel und Fettabbau im Herzen aufgeklärt. „Während die Konzentration von G0S2 nach dem Essen in der Leber sinkt, steigt sie im Herzen an“, berichtet Dr. Christoph Heier, Erstautor der aktuellen Publikation. Das wiederum führt dazu, dass weniger Fett abgebaut wird, weil G0S2 das fettspaltende Enzym ATGL (Adipose Triglyceride Lipase) hemmt“, erklärt der Forscher. Bei Nahrungsentzug sinkt der G0S2-Spiegel im Herzmuskel, die ATGL wird aktiv und der Fettabbau angekurbelt. Rudolf Zechner hat mit seinem Team 2004 die ATGL und ihre zentrale Aufgabe beim Abbau von Lipiden entdeckt. Das Enzym spaltet in Körperzellen gespeicherte Fette und versorgt auf diese Weise Gewebe und Organe mit Energie.

„Die dynamischen Veränderungen der G0S2-Konzentration helfen dem Herzmuskel, seinen Energiehaushalt flexibel an Veränderungen im Nahrungsangebot anzupassen“, fasst Christoph Heier die neuen Erkenntnisse zusammen. Wird zum Beispiel nichts gegessen, unterstützt der sinkende G0S2-Spiegel das Herz, seinen Energiehaushalt vermehrt auf Fettreserven umzustellen.

Publikation:
G0/G1 Switch Gene 2 Regulates Cardiac Lipolysis
The Journal of Biological Chemistry, Vol. 290, Issue 43, 26141-26150, October 23, 2015, doi:10.1074/jbc.M115.671842
Christoph Heier; Franz P. W. Radner; Tarek Moustafa; Renate Schreiber; Susanne Grond; Thomas O. Eichmann; Martina Schweiger; Ines K. Cerk; Monika Oberer; Robert Zimmermann; Rudolf Zechner

created by Gudrun Pichler

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