logo   Wittgenstein Award Laureate

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Gerhard J. Herndl Jan-Michael Peters Wolfgang Lutz Jürgen Knoblich Portrait Gerhard Widmer Portrait Markus Arndt Portrait Christian Krattenthaler Portrait Rudolf Zechner Portrait Joerg Schmiedmayer Portrait Barry Dickson Portrait Rudolf Grimm Portrait Walter Pohl Portrait Renee Schroeder Portrait Ferenc Krausz Portrait Heribert Hirt Portrait Meinrad Busslinger Portrait Peter Markowich Portrait Andre Gingrich Portrait Kim Ashley Nasmyth Portrait Peter Zoller Portrait Walter Schachermayer Portrait Georg Gottlob Portrait Marjori + Antonius Matzke Portrait Erich Gornik Portrait Erwin Wagner Portrait Ruth Wodak Portrait

Wittgenstein Award Laureate 2007 Univ. Prof. Dr. Rudolf Zechner

Lipid-induced Cell Dysfunction and Cell Death

Institut für Molekulare Biowissenschaften IMB ext

Rudolf Zechner, Karl Franzens University Graz, Institute of Molecular Biosciences ext

Curriculum Vitae

Publications ext

LIPOTOX ext

GOLD-GEN-AU Genomics of Lipid-associated Disorders ext

mail Contact Rudolf Zechner @mail


Summary: Research achievements of Prof. Zechner

Dr. Rudolf Zechner’s scientific work focuses on lipid and energy metabolism. This research area is of highest clinical relevance since the dysfunction of lipid metabolism is associated with particularly frequent diseases such as adiposity, type II diabetes, and atherosclerosis. The molecular mechanisms involved in the mobilization of stored lipids in cells are of particular interest for scientific research.

In 2002, the Zechner group demonstrated that established textbook knowledge about the degradation of neutral lipids needs to be corrected. Mutant mouse lines lacking the only known enzyme of cellular lipid degradation (hormone-sensitive lipase) did not show any signs of adiposity, thus indicating that an unknown additional lipase must be involved in the process. In 2004, the Zechner group discovered this enzyme and named it Adipose Triglyceride Lipase (ATGL, Science 2004). The subsequent characterization of mutant mouse lines lacking ATGL re-defined the pathway of fat degradation in mammals. These ATGL knock-out mice store high quantities of neutral fat in various body tissues and are living proof that ATGL catalyses the first step of fat degradation (Science 2006).

In further research the Zechner laboratory identified a co-activator of ATGL essential to lipid degradation in many cells (Cell Metabolism 2006). Recently, the relevance of these findings was confirmed since mutations in the ATGL gene or of its co-activator can induce severe disorders in the lipid metabolism of humans ("neutral lipid storage disease").

Summarizing, Dr. Zechner’s research group not only succeed in re-defining a pathway of lipid metabolism but also in providing the molecular basis for elucidation of genetic disorders.

Rudolf Zechner