Showing papers by "Jan F. C. Glatz published in 2001"
TL;DR: It is speculated that in obesity fatty acid transporters are relocated from an intracellular pool to the plasma membrane in heart, muscle, and adipose tissues.
274 citations
TL;DR: New evidence from in-vitro and whole-animal studies supports the existence of protein-mediated transmembrane transport of FAs, which is likely to coexist with passive diffusional uptake.
Abstract: Cellular long-chain fatty acid (FA) transport and metabolism are believed to be regulated by membrane-associated and soluble proteins that bind and transport FAs. Several different classes of membrane proteins have been proposed as FA acceptors or transmembrane FA transporters. New evidence from in-vitro and whole-animal studies supports the existence of protein-mediated transmembrane transport of FAs, which is likely to coexist with passive diffusional uptake. The trafficking of FAs by intracellular fatty acid-binding proteins may involve their interaction with specific membrane or protein targets. Evidence is also emerging for concerted actions between the membrane and cytoplasmic fatty acid-binding proteins that allow for efficient regulation of FA transport and metabolism.
152 citations
TL;DR: Evidence is presented that in skeletal muscle, fatty acid uptake is subject to short-term regulation by translocation of FAT/CD36 from intracellular stores to the plasma membrane, analogous to the regulation of muscular glucose uptake by GLUT-4 translocation.
Abstract: The transport of long-chain fatty acids across cellular membranes most likely occurs to some extent by passive diffusion and additionally is facilitated by a number of membrane-associated and cytoplasmic proteins. In this overview we focus on the involvement of the membrane proteins fatty acid translocase (FAT/CD36), plasma membrane fatty acid-binding protein (FABPpm) and fatty acid-transport protein (FATP). Newly obtained evidence is presented that in skeletal muscle, fatty acid uptake is subject to short-term regulation by translocation of FAT/CD36 from intracellular stores to the plasma membrane, analogous to the regulation of muscular glucose uptake by GLUT-4 translocation. These new findings establish a significant role of membrane-associated proteins in the cellular fatty acid-uptake process. Possible implications for the uptake and transport of long-chain fatty acids by the brain are discussed.
70 citations
TL;DR: In a new model system (giant vesicles), it is demonstrated that LCFA transport rates are scaled with the oxidative capacity of heart and muscle andLCFA transport can be increased by increasing the FAT/CD36 protein of muscle.
Abstract: While it has long been assumed that long chain fatty acids (LCFA) can freely diffuse across the plasma membrane, recent work has shown that LCFA uptake also involves a protein-mediated mechanism. Three putative LCFA transporters have been identified (FABPpm, FATP, and FAT/CD36), and all are expressed in rodent and human muscles. In a new model system (giant vesicles), we have demonstrated that (a) LCFA transport rates are scaled with the oxidative capacity of heart and muscle, (b) only FABPpm and FAT/CD36, but not FATP1, correlate with vesicular LCFA transport, and (c) LCFA transport can be increased by increasing (1) the FAT/CD36 protein of muscle (chronic adaptation) or (2) via the translocation of FAT/CD36 from an intracellular pool to the plasma membrane during muscle contraction (acute adaptation).
48 citations
TL;DR: The adult rat heart responds to changes in nutritional status, as provoked by 46 h fasting, through adjustment of glucose as well as FA metabolism at the level of gene expression.
48 citations
TL;DR: The ability to increase muscle FABPc could be directly related to weight loss and to changes in fat oxidation following dietary intervention in obesity and Type II (non-insulin-dependent) diabetes mellitus.
Abstract: Aims/hypothesis:
There is increasing evidence that intracellular fatty acid binding proteins (FABPc's; 15 kD) function as vehicles of cytosolic fatty acid transport. We studied skeletal muscle cytosolic FABPc, and enzymes reflecting β-oxidation and oxidative capacity (3-hydroxyacyl-CoA dehydrogenase, HAD, and citrate synthase, CS) in relation to weight loss and changes in substrate utilisation in a group of 35 obese women and obese men with Type II (non-insulin-dependent) diabetes mellitus (women = 27, men = 8).
15 citations
01 Jan 2001
TL;DR: Binding Protein: rapid testing and diagnostic value and its application in clinical practice.
Abstract: Binding Protein: rapid testing and diagnostic valueHelma Kaptein, Cangel Chan, John Sanderson, Jan Glatz, Wing Leung1, Reinhard Renneberg1 1 Department of Chemistry, The Hong Kong University of Science and Technology, Clear Water Bay Kowloon, Hong Kong 2 Department of Medicine and Therapeutics, The Chinese University of Hong Kong Sha Tin, Hong Kong 3 CARIM Institute, University of Maastricht Maastricht, The Netherlands chrenneb@ust.hk Registriernummer der Online-Anmeldung: 335
6 citations