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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.

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Journal ArticleDOI

Plasma heart-type fatty acid binding protein is superior to troponin and myoglobin for rapid risk stratification in acute pulmonary embolism.

TL;DR: H-FABP measured on admission is useful for short-term risk stratification in APE and appears to be superior to cTnT, NT-proBNP and Mb in the prediction of 30-day APE-related mortality.
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New insights into long-chain fatty acid uptake by heart muscle: a crucial role for fatty acid translocase/CD36

TL;DR: The fatty acid transporting role of FAT/ CD36 is further demonstrated in mice overexpressing muscle-specific FAT/CD36, and in transgenic mice generated using a genetic-rescue approach.
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Requirement for distinct vesicle-associated membrane proteins in insulin- and AMP-activated protein kinase (AMPK)-induced translocation of GLUT4 and CD36 in cultured cardiomyocytes

TL;DR: The involvement of distinct VAMP isoforms in both GLUT4 and CD36 translocation indicates that CD 36 translocation is a vesicle-mediated process dependent on soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex formation.
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In obese rat muscle transport of palmitate is increased and is channeled to triacylglycerol storage despite an increase in mitochondrial palmitate oxidation

TL;DR: Fatty acid transport, esterification, and oxidation are upregulated in muscles of obese Zucker rats, with these effects being most pronounced in red muscle, suggesting that upregulation in fatty acid transport as opposed to altered fatty acid oxidation is the major determinant of intramuscular lipid accumulation.
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The subcellular compartmentation of fatty acid transporters is regulated differently by insulin and by AICAR

TL;DR: There appears to be tissue‐specific sensitivity to insulin‐induced FATP1 translocation, as it has been shown elsewhere that insulin induces FATP 1 translocation in 3T3‐L1 adipocytes, and clearly, the subcellular distribution of FABPpm is acutely regulated in cardiac myocytes, although FABppm and FAT/CD36 do not necessarily respond identically to the same stimuli.