Focus on EAS Innsbruck 2016: Introducing the faculty - Plenary speaker Rudolf Zechner
14 December 2015
A forward-looking scientific Programme to excite, inspire and inform!
The EAS 2016 Scientific Committee has created a programme featuring ground-breaking speakers in their respective fields. EAS 2016 Innsbruck welcomes a distinguished international faculty to share their forward-looking perspectives on the latest developments in basic research and clinical practice in atherosclerosis and cardiovascular disease. You can find details of the Plenary and Workshop sessions now on the Congress website, www.eas2016.kenes.com.
Abstract submission is now open. Submit your abstract by January 11, 2016 for the opportunity to present your findings at this prestigious international Congress.
Here, in a series of newsletters, we introduce members of the EAS 2016 Innsbruck faculty.
Plenary session 2, Tuesday, May 31, 2016: Lipid biology, new insights
Rudolf Zechner, Austria: Pathophysiology of intracellular and intravascular lipolysis
Rudolf Zechner is Professor of Biochemistry, the Institute of Molecular Biosciences at the University of Graz, Austria. Professor Zechner obtained his Ph.D. in chemistry from the University of Graz, followed by postdoc-toral studies at the Medical School of this university, before working as a Research Associate at the Labora-tory of Biochemical Genetics and Metabolism, Rockefeller University, New York, USA. His contributions to the field of lipid metabolism include investigation of the physiological role of lipoprotein lipase and the func-tion of hormone-sensitive lipase during fat cell lipolysis, and the discovery of adipose-triglyceride lipase (ATGL) and its coactivator protein CGI-58. ATGL/CGI-58-mediated triglyceride hydrolysis represents the rate-limiting step in fat catabolism in adipose and non-adipose tissues. Ongoing research in his laboratory is focused on understanding the mechanisms underlying the lipolytic process, defining the role of lipolysis in lipid-mediated signal transduction, and investigating the role of lipolysis in cancer and cancer-associated cachexia. Professor Zechner was awarded the 2015 Louis-Jeantet Prize for Medicine for his work in the field of lipid and energy metabolism.
All organisms use fatty acids (FAs) for energy substrates and as precursors for membrane and signalling lipids; however, triglycerides (TGs), the form in which FAs are transported and stored, are not able to cross the cell membrane. Lipolysis is key to this process. Recent discoveries, including that of glycosylphosphati-dylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1), the molecule that moves lipo-protein lipase (LPL) from the interstitial spaces to the capillary lumen, and adipose triglyceride lipase (ATGL) and comparative gene identification-58 (CGI-58), key to the hydrolysis of TGs within cells, have extended understanding of the underlying mechanisms. Despite this, a number of questions remain, including the molecular basis for LPL–GPIHBP1 interactions, as well as the possibility that this molecule may play a role in the margination of triglyceride-rich lipoproteins along the surface of capillaries.
Two other enzymes of the same family, hepatic lipase (HL) and endothelial lipase (EL), participate in the remodelling of plasma lipoproteins. The physiologic roles of these lipases are less well defined. Evidence to date implies that HL and EL fine-tune a complex system of lipoprotein processing, thus affecting the deliv-ery of lipid nutrients to specific cell types.
Considering the central role of lipases in lipid and energy metabolism, it is not surprising that they have proven to be relevant to human disease. Indeed, a potential role of lipolysis in the development of obesity and insulin resistance has been suggested. Lipases have also been shown to affect tumour proliferation. These insights stimulate ongoing research into their therapeutic potential for a range of conditions, includ-ing the treatment of insulin resistance and type 2 diabetes.
Schweiger M, Zechner R. Breaking the barrier--Chaperone-mediated autophagy of perilipins regulates the lipolytic degradation of fat. Cell Metab 2015;22:60-1.
Schreiber R, Hofer P, Taschler U, Voshol PJ, Rechberger GN, Kotzbeck P, Jaeger D, Preiss-Landl K, Lord CC, Brown JM, Haemmerle G, Zimmermann R, Vidal-Puig A, Zechner R. Hypophagia and metabolic adaptations in mice with defective ATGL-mediated lipolysis cause resistance to HFD-induced obesity. Proc Natl Acad Sci U S A 2015 Oct 27. pii: 201516004. [Epub ahead of print]
Heier C, Radner FP, Moustafa T, Schreiber R, Grond S, Eichmann TO, Schweiger M, Schmidt A, Cerk IK, Oberer M, Theussl HC, Wojciechowski J, Penninger JM, Zimmermann R, Zechner R. G0/G1 Switch Gene 2 regulates cardiac lipolysis. J Biol Chem 2015;290:26141-50.