Biochemistry and molecular genetics
J.J.F.P. Luiken, PhD
PO Box 616
6200 MD Maastricht
T: (+31) (0)43 3881209
Joost J.F.P. Luiken, PhD studied biology at the University of Utrecht and graduated in 1988, specialized in biochemistry and molecular genetics. After military service and a PhD-project on liver metabolism at the Univeristy of Amsterdam, he started working at Maastricht University as post-doc in November 1994 to study the role of fatty acid transporters in the heart. Starting in 1997, he worked for two and a half years in the laboratory of prof. Bonen, University of Waterloo, Canada, to learn novel techniques to study fatty acid uptake by muscle tissues. In June 1999, he returned to Maastricht on a postdoctoral Dekker stipendium of the Netherlands Heart Foundation to introduce these novel techniques, first in the department of Physiology and since 2003 in the department of Molecular Genetics. In 2000, he won the prestigious FASEB-award on Endocrinology and Metabolism for his discovery of a novel mechanism of acute regulation of fatty acid uptake via translocation of fatty acid transporters from intracellular stores to the cell surface. In 2002, he was awarded a VIDI-grant to continue his research on the identification of the cellular machinery involved in fatty acid transporter translocation and to study the role of fatty acid transporters in cardiac disease (diabetic cardiomyopathy). In 2008, he was appointed as staff member of the department of Molecular Genetics.
Upon his initial discoveries that (i) CD36 is the predominant fatty acid transporter in the heart, and (ii) CD36 activity is regulated by reversible translocation from intracellular stores (endosomes) to the sarcolemma, Joost Luiken discovered that in the rodent diabetic heart CD36 is permanently relocated from the endosomes to the sarcolemma without changes in expression. The increase in cell surface abundance of CD36 will lead to chronically increased myocardial fatty acid uptake, lipid accumulation, insulin resistance, and finally cardiac dysfunction. Further research on the causes of this aberrant CD36 subcellular localization brought forward that alterations in the CD36-dedicated trafficking machinery are responsible for sarcolemmal CD36 relocation. Because the CD36-dedicated trafficking machinery is completely unexplored, his recent studies focused on screening for and identifying CD36-dedicated trafficking proteins, and their altered functioning in the diabetic heart.
Yilin Liu, Laura K.M. Steinbusch, Miranda Nabben, Dimitris Kapsokalyvas, Marc van Zandvoort, Patrick Schönleitner, Gudrun Antoons, Peter J. Simons, Will A. Coumans, Amber Geomini, Dipanjan Chanda, Jan F.C. Glatz, Dietbert Neumann, Joost J.F.P. Luiken. Palmitate-Induced Vacuolar-Type H+-ATPase Inhibition Feeds Forward Into Insulin Resistance and Contractile Dysfunction. Diabetes 2017; 66:1521–1534.
Luiken JJFP, Koonen DPY, Willems J, Zorzano A, Becker C, Fischer Y, Tandon NN, Van der Vusse GJ, Bonen A, Glatz JFC. Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. Diabetes 51: 3113-3119, 2002.
Luiken JJFP, Coort SLM, Willems J, Coumans WA, Bonen A, Van der Vusse GJ, Glatz JFC. Contraction-induced fatty acid translocase/CD36 translocation in rat cardiac myocytes is mediated through AMP-activated protein kinase signaling. Diabetes 52: 1627-1634.
Ouwens DM, Diamant M, Fodor M, Habets DDJ, Pelsers MMAL, El Hasnaoui M, Dang ZC, van den Brom CE, Vlasblom R, Boer C, Coort SLM, Glatz JFC, Luiken JJFP. Cardiac contractile dysfunction in insulin resistant high-fat diet fed rats associates with elevated CD36-mediated fatty acid uptake and esterification. Diabetologia. 50: 1938-1948.
Glatz JFC, Luiken JJFP, Bonen A. Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. Physiol Rev. 90: 367-417.
Steinbusch LKM, Dirkx E, Hoebers NT, Roelants V, Foretz M, Viollet B, Diamant M, van Eys G, Ouwens DM, Bertrand L, Glatz JFC, Luiken JJFP. Overexpression of AMP-activated protein kinase or protein kinase D prevents lipid-induced insulin resistance in cardiomyocytes. J Mol Cell Cardiol. 55:165-73.