Rudolf Zechner
University of Graz
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Primary Section: 42, Medical Physiology and Metabolism Membership Type:
International Member
(elected 2019)
Photo Credit: Joel Kernasenko |
Biosketch
Rudolf Zechner is a biochemist working in the field of lipid and energy metabolism. He is most recognized for the discovery of adipose triglyceride lipase, which is a key enzyme for the catabolism of fat in all vertebrates. Rudolf Zechner was born and educated in Graz, Austria. He graduated from the University of Graz with a PhD degree in chemistry in 1980. Zechner was a post-doctoral fellow at the Laboratory of Biochemical Genetics and Metabolism at the Rockefeller University in New York. After his return to Europe, he became associate professor at the Institute of Medical Biochemistry and in 1998 full professor of biochemistry at the Institute of Molecular Biosciences at the University of Graz, Austria. Since 2016, he is the director of BioTechMed-Graz, a research cooperation between three Universities in the field of biomedicine. Zechner is the recipient of the Wittgenstein Prize (Austria), an ERC Advanced Grant, and the Louis Jeantet Prize for Medicine and is also a member of the Austrian Academy of Sciences. In 2019 he was elected as foreign associate of the National Academy of Sciences, USA.
Research Interests
Rudolf Zechner studies the mechanisms regulating lipid metabolism and causes of metabolic diseases. His team specifically focuses on fat-degrading enzymes called lipases. Discovery of adipose triglyceride lipase and the demonstration that this enzyme initiates fat catabolism in mice and humans overturned our understanding of the lipolytic pathway. More recently, Zechner's laboratory investigates how the breakdown of fat affects cellular signaling processes and cell function. Discoveries of the Zechner laboratory identified crucial links between fat catabolism, nuclear receptor signaling and heart function or the role of lipolysis in thermogenesis. Current work focuses on the functional impact of lipolysis in the pathogenesis of cancer-associated cachexia, a fatal wasting disease that is characterized by the unintended loss of body weight. Furthermore, the finding that pharmacological inhibition of adipose triglyceride lipase reduces high fat diet-induced obesity, glucose intolerance, and liver steatosis in mice, drives current efforts to probe the enzyme's potential as a therapeutic target to treat obesity-related metabolic disorders.
