Prof. Jan Glatz

Head Genetics and Cell Biology, head Molecular Genetics

Focus areas

Professor of Metabolic Aspects of Cardiovascular Diseases, biochemist/physiologist


Prof. J.F.C. Glatz
Maastricht University
Molecular Genetics
PO Box 616
6200 MD Maastricht
T: (+31) (0)43 3881998

Curriculum vitae

Jan Glatz (1955) studied chemistry and biochemistry (Nijmegen and Utrecht) and received his PhD degree from Nijmegen University in 1983 on the basis of a thesis on fatty acid metabolism in cardiac and skeletal muscle. Following a post-doctoral period in Human Nutrition at Wageningen University, he joined Maastricht University in 1986 to be trained as molecular physiologist and study cardiac lipid uptake and metabolism. In 1990 he became Established Investigator of the Netherlands Heart Foundation and in 2003 was appointed as (the first) Netherlands Heart Foundation Professor.

Currently he is full professor of Cardiac Metabolism studying the regulation of energy metabolism in the healthy and diabetic heart, with focus on membrane substrate transporters and their application for so-called metabolic modulation therapy.

Prof. Glatz is (co)author of >330 publications of which 28 (mostly invited) reviews. His publications have received >11,000 citations; his Hirsch factor is 55. He also is co-founder and Chief Scientific Officer (CSO) of the small biotech company FABPulous (point-of-care diagnostics).

In 2012 he was appointed as President of the Society for Heart and Vascular Metabolism (SHVM). Previously he served on the Board of Directors of the International Society for the Study of Fatty Acids and Lipids (ISSFAL), and of the Steering Committee of the International Conferences on the Biosciences of Lipids (ICBL). He was the initiator of a series of international conferences on lipid binding proteins (held since 1989) and was (co-)organizer of >20 international conferences held in Maastricht, a.o. 5th SHVM (2008), 49th ICBL (2008), 9th ISSFAL (2010).

Cardiac energy metabolism and chronic cardiac disease

The aim of the programme is to disclose the mechanisms underlying the process of metabolic (mal)adaptation and its relation to cardiac (dys)function in pathophysiological conditions such as diabetic cardiomyopathy (DCM) and Wolff-Parkinson-White (WPW) syndrome (glycogen storage disease). DCM is common in type 2 diabetes and results from the adaptation of the insulin-resistant heart towards an increased utilization of fatty acids for energy production, at the expense of glucose. The increased fatty acid uptake rate leads to intracellular accumulation of lipids and toxic lipid intermediates (lipotoxicity) which aggravate insulin resistance (further diminished glucose uptake) and mitochondrial function, leading to severe cardiac dysfunction. Central in the research program are (i) the roles of external and environmental factors (cytokines, high-fat diet, etc.) in the development of DCM, and (ii) the development of strategies to normalize the substrate balance in the diabetic heart, i.e., lower fatty acid uptake and increase glucose utilization (‘metabolic modulation’), by manipulating the sarcolemmal presence and activity of substrate transporters for fatty acids and for glucose, and by reducing the adverse affects of substrate intermediates on mitochondrial function. In the WPW syndrome glycogen utilization is impaired which becomes manifest in a markedly reduced (flexibility of) cardiac function. The hypothesis is studied that this is the result of a defect in the interaction between AMP kinase and glycogen.

Research group: Joost J.F.P. Luiken, PhD, Dietbert Neumann, PhD, Will A. Coumans, Dipanjan Chanda, PhD, Ricardo Rodriguez Calvo, PhD, Yvonne Oligschläger, PhD, Marie Miglianico, Xiaoqing Zhu, Yilin Liu
School: CARIM

Publications (selection)

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.

Pelsers MMAL, Hermens WT, Glatz JFC. Fatty acid-binding proteins as plasma markers of tissue injury. Clin Chim Acta 352: 15-35, 2005.

Glatz JFC, Luiken JJFP, Bonen A. Membrane fatty acid transporets as regulators of lipid metabolism (Review). Physiol Rev 90: 367-417, 2010.

Dirkx E, Schwenk RW, Coumans WA, Hoebers N, Angin Y, Viollet B, Bonen A, Van Eys GJJM, Glatz JFC, Luiken JJFP. Protein kinase D1 is essential for contraction-induced glucose uptake, but is not involved in fatty acid uptake into cardiomyocytes. J Biol Chem 287: 5871-5881, 2012

Glatz JFC, Angin Y, Steinbusch LKM, Schwenk RW, Luiken JJFP. CD36 as target to prevent cardiac lipotoxicity and insulin resistance. Prostagl Leukotr Essent Fatty Acids 88: 71-77, 2013

Chen L, Xin F-J, Wang J, Hu J, Zhang Y-Y, Wan S, Cao L-S, Lu C, Li P, Yan SF, Neumann D, Schlattner U, Xia B, Wang Z-X, Wu J-W. Conserved regulatory elements in AMPK. Nature 498: E8-E10, 2013

Social media