J
Jan F. C. Glatz
Researcher at Maastricht University
Publications - 309
Citations - 20133
Jan F. C. Glatz is an academic researcher from Maastricht University. The author has contributed to research in topics: Fatty acid & CD36. The author has an hindex of 72, co-authored 304 publications receiving 18662 citations. Previous affiliations of Jan F. C. Glatz include Maastricht University Medical Centre & Leiden University Medical Center.
Papers
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Journal ArticleDOI
Protein-mediated Fatty Acid Uptake in the Heart
TL;DR: The evidence indicating that LCFA transport into the heart involves a protein-mediated mechanism is examined, the proteins involved in this process, including FAT/CD36, FABPpm and FATP1 are discussed, and the mechanisms involved in regulating LCFAs transport by some of these proteins are discussed.
Journal ArticleDOI
Signaling pathways involved in cardiac energy metabolism
TL;DR: This review focuses on recent advances on the role of these signaling pathways and transcription factors involved in the regulation of CD36 and GLUT4.
Journal ArticleDOI
Diagnostic value of a heart-type fatty acid-binding protein (H-FABP) bedside test in suspected acute coronary syndrome in primary care.
M.H.E. Bruins Slot,Frans H. Rutten,G.J.M.G. van der Heijden,P. A. F. M. Doevendans,E.G. Mast,Ad C. Bredero,O.P. van der Spoel,Jan F. C. Glatz,Arno W. Hoes +8 more
TL;DR: The H-FABP rapid test cannot be used to safely exclude rule out ACS and can only be used safely in patients otherwise NOT referred to hospital by the GP, as an extra precaution not to miss ACS.
Journal ArticleDOI
Fatty acid transport and transporters in muscle are critically regulated by Akt2.
Swati S. Jain,Joost J. F. P. Luiken,Laelie A. Snook,Xiao-Xia Han,Graham P. Holloway,Jan F. C. Glatz,Arend Bonen +6 more
TL;DR: In muscle fromAkt2‐knockout mice, it is observed that Akt2 is critically involved in both insulin‐induced and contraction‐induced fatty acid transport and translocation of fatty acid translocase/CD36 (CD36) and FATP1, but not of translocationof fatty acid‐binding protein (FABPpm) and fat acid transporters.
Journal ArticleDOI
Protein kinase-D1 overexpression prevents lipid-induced cardiac insulin resistance.
Ellen Dirkx,Guillaume J.J.M. van Eys,Robert W. Schwenk,Laura K.M. Steinbusch,Nicole Hoebers,Will A. Coumans,Tim Peters,Ben J. A. Janssen,Boudewijn Brans,Andreas T. Vogg,Dietbert Neumann,Jan F. C. Glatz,Joost J. F. P. Luiken +12 more
TL;DR: Data suggest that PKD pathway activation may be an attractive therapeutic strategy to mitigate lipid accumulation, insulin resistance and maladaptive remodeling in the lipid-overloaded heart, but this requires further investigation.