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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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Cardiac contraction-induced GLUT4 translocation requires dual signaling input.

TL;DR: Contraction-induced translocation of glucose transporter type-4 (GLUT4) to the sarcolemma is essential to stimulate cardiac glucose uptake during increased energy demand and this process is a target for therapeutic strategies aiming at increasing glucose uptake in insulin-resistant and/or diabetic hearts.
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A new principle for rapid immunoassay of proteins based on in situ precipitate-enhanced ellipsometry.

TL;DR: Quantitative validation was obtained by use of annexin V, a protein with high binding affinity for phosphatidylserine-containing phospholipid membranes, resulting in a transport-limited adsorption rate, and a possible future application of the method in the development of a one-step ELISA is discussed.
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Restoring AS160 phosphorylation rescues skeletal muscle insulin resistance and fatty acid oxidation while not reducing intramuscular lipids

TL;DR: The rapid AICAR- and leptin-mediated rescue of palmitate-induced insulin resistance is attributable to the restoration of insulin-stimulated AS160 phosphorylation and GLUT4 translocation.
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Novel “Digital‐Style” Rapid Test Simultaneously Detecting Heart Attack and Predicting Cardiovascular Disease Risk

TL;DR: A novel “digital‐style” semiquantitative lateral flow assay simultaneously detecting heart attack and predicting early cardiovascular disease risk, just by simply counting the number of red lines in the test without any expensive reading instrument has been successfully developed.
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Caffeine‐stimulated fatty acid oxidation is blunted in CD36 null mice

TL;DR: This work examined whether this increase in fatty acid oxidation was attributable to a calcium‐induced translocation of the fatty acid transporter CD36 to the sarcolemma, thereby providing an enhanced influx of fatty acids to increase their oxidation.