The Experts below are selected from a list of 231 Experts worldwide ranked by ideXlab platform
Joost J. F. P. Luiken - One of the best experts on this subject based on the ideXlab platform.
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Fatty Acid transport across the cell membrane: Regulation by Fatty Acid transporters
Prostaglandins Leukotrienes and Essential Fatty Acids, 2010Co-Authors: Robert W. Schwenk, Graham P. Holloway, Joost J. F. P. Luiken, Arend Bonen, Jan F. C. GlatzAbstract:Abstract Transport of long-chain Fatty Acids across the cell membrane has long been thought to occur by passive diffusion. However, in recent years there has been a fundamental shift in understanding, and it is now generally recognized that Fatty Acids cross the cell membrane via a protein-mediated mechanism. Membrane-associated Fatty Acid-binding proteins (‘Fatty Acid transporters') not only facilitate but also regulate cellular Fatty Acid uptake, for instance through their inducible rapid (and reversible) translocation from intracellular storage pools to the cell membrane. A number of Fatty Acid transporters have been identified, including CD36, plasma membrane-associated Fatty Acid-binding protein (FABP pm ), and a family of Fatty Acid transport proteins (FATP1–6). Fatty Acid transporters are also implicated in metabolic disease, such as insulin resistance and type-2 diabetes. In this report we briefly review current understanding of the mechanism of transmembrane Fatty Acid transport, and the function of Fatty Acid transporters in healthy cardiac and skeletal muscle, and in insulin resistance/type-2 diabetes. Fatty Acid transporters hold promise as a future target to rectify lipid fluxes in the body and regain metabolic homeostasis.
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rosiglitazone increases Fatty Acid oxidation and Fatty Acid translocase fat cd36 but not carnitine palmitoyltransferase i in rat muscle mitochondria
The Journal of Physiology, 2008Co-Authors: Carley R Benton, Graham P. Holloway, Joost J. F. P. Luiken, Jan F. C. Glatz, S E Campbell, Yuko Yoshida, Narendra N Tandon, Lawrence L Spriet, Arend BonenAbstract:Peroxisome proliferator-activated receptors (PPARs) alter the expression of genes involved in regulating lipid metabolism. Rosiglitazone, a PPARγ agonist, induces tissue-specific effects on lipid metabolism; however, its mode of action in skeletal muscle remains unclear. Since Fatty Acid translocase (FAT/CD36) was recently identified as a possible regulator of skeletal muscle Fatty Acid transport and mitochondrial Fatty Acid oxidation, we examined in this tissue the effects of rosiglitazone infusion (7 days, 1 mg day−1) on FAT/CD36 mRNA and protein, its plasmalemmal content and Fatty Acid transport. In addition, in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria we examined rates of Fatty Acid oxidation, FAT/CD36 and carnitine palmitoyltransferase I (CPTI) protein, and CPTI and β-hydroxyacyl CoA dehydrogenase (β-HAD) activities. Rosiglitazone did not alter FAT/CD36 mRNA or protein expression, FAT/CD36 plasmalemmal content, or the rate of Fatty Acid transport into muscle (P > 0.05). In contrast, rosiglitazone increased the rates of Fatty Acid oxidation in both SS (+21%) and IMF mitochondria (+36%). This was accompanied by concomitant increases in FAT/CD36 in subsarcolemmal (SS) (+43%) and intermyofibrillar (IMF) mitochondria (+46%), while SS and IMF CPTI protein content, and CPTI submaximal and maximal activities (P > 0.05) were not altered. Similarly, citrate synthase (CS) and β-HAD activities were also not altered by rosiglitazone in SS and IMF mitochondria (P > 0.05). These studies provide another example whereby changes in mitochondrial Fatty oxidation are associated with concomitant changes in mitochondrial FAT/CD36 independent of any changes in CPTI. Moreover, these studies identify for the first time a mechanism by which rosiglitazone stimulates Fatty Acid oxidation in skeletal muscle, namely the chronic, subcellular relocation of FAT/CD36 to mitochondria.
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exercise and insulin increase muscle Fatty Acid uptake by recruiting putative Fatty Acid transporters to the sarcolemma
Current Opinion in Clinical Nutrition and Metabolic Care, 2002Co-Authors: Jan F. C. Glatz, Arend Bonen, Joost J. F. P. LuikenAbstract:Purpose of review Skeletal muscle metabolic energy, needed to maintain contractile activity, is mainly obtained from glucose and long-chain Fatty Acids. Recent studies have revealed a remarkable parallel between the regulation of uptake of glucose and Fatty Acids by muscle, in that each is mediated by sarcolemmal transporters that are recruited from an intracellular storage site. The focus of this review is to describe newly obtained insights on the recruitment of Fatty Acid transporters and their malfunctioning in diabetes. Recent findings The major Fatty Acid transporter involved is Fatty Acid translocase (CD36). Translocation of this protein to the membrane is triggered by muscle contraction and by insulin, and presumably occurs from distinct intracellular pools. This resembles the well documented exercise and insulin-induced recruitment of glucose transporter-4. Whether another transporter, plasma membrane Fatty Acid-binding protein, is also subject to such recycling is not yet clear. In a rodent model of insulin-dependent (type 1) diabetes, the increased rate of muscle Fatty Acid uptake could be associated with an increased total amount of Fatty Acid translocase (CD36). In a model of non-insulin dependent (type 2) diabetes, this increased rate could be associated with a permanent relocalization of Fatty Acid translocase to the sarcolemma. Summary These findings indicate a pivotal role for the membrane transporter Fatty Acid translocase in the exercise and insulin-induced increases of muscle Fatty Acid uptake and utilization, and suggest that malfunctioning of the cellular recycling of Fatty Acid translocase is involved in the etiology of insulin resistance and type 2 diabetes.
Jan F. C. Glatz - One of the best experts on this subject based on the ideXlab platform.
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Fatty Acid transport across the cell membrane: Regulation by Fatty Acid transporters
Prostaglandins Leukotrienes and Essential Fatty Acids, 2010Co-Authors: Robert W. Schwenk, Graham P. Holloway, Joost J. F. P. Luiken, Arend Bonen, Jan F. C. GlatzAbstract:Abstract Transport of long-chain Fatty Acids across the cell membrane has long been thought to occur by passive diffusion. However, in recent years there has been a fundamental shift in understanding, and it is now generally recognized that Fatty Acids cross the cell membrane via a protein-mediated mechanism. Membrane-associated Fatty Acid-binding proteins (‘Fatty Acid transporters') not only facilitate but also regulate cellular Fatty Acid uptake, for instance through their inducible rapid (and reversible) translocation from intracellular storage pools to the cell membrane. A number of Fatty Acid transporters have been identified, including CD36, plasma membrane-associated Fatty Acid-binding protein (FABP pm ), and a family of Fatty Acid transport proteins (FATP1–6). Fatty Acid transporters are also implicated in metabolic disease, such as insulin resistance and type-2 diabetes. In this report we briefly review current understanding of the mechanism of transmembrane Fatty Acid transport, and the function of Fatty Acid transporters in healthy cardiac and skeletal muscle, and in insulin resistance/type-2 diabetes. Fatty Acid transporters hold promise as a future target to rectify lipid fluxes in the body and regain metabolic homeostasis.
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rosiglitazone increases Fatty Acid oxidation and Fatty Acid translocase fat cd36 but not carnitine palmitoyltransferase i in rat muscle mitochondria
The Journal of Physiology, 2008Co-Authors: Carley R Benton, Graham P. Holloway, Joost J. F. P. Luiken, Jan F. C. Glatz, S E Campbell, Yuko Yoshida, Narendra N Tandon, Lawrence L Spriet, Arend BonenAbstract:Peroxisome proliferator-activated receptors (PPARs) alter the expression of genes involved in regulating lipid metabolism. Rosiglitazone, a PPARγ agonist, induces tissue-specific effects on lipid metabolism; however, its mode of action in skeletal muscle remains unclear. Since Fatty Acid translocase (FAT/CD36) was recently identified as a possible regulator of skeletal muscle Fatty Acid transport and mitochondrial Fatty Acid oxidation, we examined in this tissue the effects of rosiglitazone infusion (7 days, 1 mg day−1) on FAT/CD36 mRNA and protein, its plasmalemmal content and Fatty Acid transport. In addition, in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria we examined rates of Fatty Acid oxidation, FAT/CD36 and carnitine palmitoyltransferase I (CPTI) protein, and CPTI and β-hydroxyacyl CoA dehydrogenase (β-HAD) activities. Rosiglitazone did not alter FAT/CD36 mRNA or protein expression, FAT/CD36 plasmalemmal content, or the rate of Fatty Acid transport into muscle (P > 0.05). In contrast, rosiglitazone increased the rates of Fatty Acid oxidation in both SS (+21%) and IMF mitochondria (+36%). This was accompanied by concomitant increases in FAT/CD36 in subsarcolemmal (SS) (+43%) and intermyofibrillar (IMF) mitochondria (+46%), while SS and IMF CPTI protein content, and CPTI submaximal and maximal activities (P > 0.05) were not altered. Similarly, citrate synthase (CS) and β-HAD activities were also not altered by rosiglitazone in SS and IMF mitochondria (P > 0.05). These studies provide another example whereby changes in mitochondrial Fatty oxidation are associated with concomitant changes in mitochondrial FAT/CD36 independent of any changes in CPTI. Moreover, these studies identify for the first time a mechanism by which rosiglitazone stimulates Fatty Acid oxidation in skeletal muscle, namely the chronic, subcellular relocation of FAT/CD36 to mitochondria.
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exercise and insulin increase muscle Fatty Acid uptake by recruiting putative Fatty Acid transporters to the sarcolemma
Current Opinion in Clinical Nutrition and Metabolic Care, 2002Co-Authors: Jan F. C. Glatz, Arend Bonen, Joost J. F. P. LuikenAbstract:Purpose of review Skeletal muscle metabolic energy, needed to maintain contractile activity, is mainly obtained from glucose and long-chain Fatty Acids. Recent studies have revealed a remarkable parallel between the regulation of uptake of glucose and Fatty Acids by muscle, in that each is mediated by sarcolemmal transporters that are recruited from an intracellular storage site. The focus of this review is to describe newly obtained insights on the recruitment of Fatty Acid transporters and their malfunctioning in diabetes. Recent findings The major Fatty Acid transporter involved is Fatty Acid translocase (CD36). Translocation of this protein to the membrane is triggered by muscle contraction and by insulin, and presumably occurs from distinct intracellular pools. This resembles the well documented exercise and insulin-induced recruitment of glucose transporter-4. Whether another transporter, plasma membrane Fatty Acid-binding protein, is also subject to such recycling is not yet clear. In a rodent model of insulin-dependent (type 1) diabetes, the increased rate of muscle Fatty Acid uptake could be associated with an increased total amount of Fatty Acid translocase (CD36). In a model of non-insulin dependent (type 2) diabetes, this increased rate could be associated with a permanent relocalization of Fatty Acid translocase to the sarcolemma. Summary These findings indicate a pivotal role for the membrane transporter Fatty Acid translocase in the exercise and insulin-induced increases of muscle Fatty Acid uptake and utilization, and suggest that malfunctioning of the cellular recycling of Fatty Acid translocase is involved in the etiology of insulin resistance and type 2 diabetes.
Sepp D Kohlwein - One of the best experts on this subject based on the ideXlab platform.
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Fatty Acid synthesis and elongation in yeast
Biochimica et Biophysica Acta, 2007Co-Authors: Oksana Tehlivets, Kim Scheuringer, Sepp D KohlweinAbstract:Abstract Fatty Acids are essential compounds in the cell. Since the yeast Saccharomyces cerevisiae does not feed typically on Fatty Acids, cellular function and growth relies on endogenous synthesis. Since all cellular organelles are involved in – or dependent on – Fatty Acid synthesis, multiple levels of control may exist to ensure proper Fatty Acid composition and homeostasis. In this review, we summarize what is currently known about enzymes involved in cellular Fatty Acid synthesis and elongation, and discuss potential links between Fatty Acid metabolism, physiology and cellular regulation.
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Fatty Acid synthesis and elongation in yeast
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids, 2007Co-Authors: Oksana Tehlivets, Kim Scheuringer, Sepp D KohlweinAbstract:Fatty Acids are essential compounds in the cell. Since the yeast Saccharomyces cerevisiae does not feed typically on Fatty Acids, cellular function and growth relies on endogenous synthesis. Since all cellular organelles are involved in - or dependent on - Fatty Acid synthesis, multiple levels of control may exist to ensure proper Fatty Acid composition and homeostasis. In this review, we summarize what is currently known about enzymes involved in cellular Fatty Acid synthesis and elongation, and discuss potential links between Fatty Acid metabolism, physiology and cellular regulation. © 2006 Elsevier B.V. All rights reserved.
Karen Freijanes Presmanes - One of the best experts on this subject based on the ideXlab platform.
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Analysis of interspecific variation in relative Fatty Acid composition: use of flow cytometry to estimate unsaturation index and relative polyunsaturated Fatty Acid content in microalgae
Journal of Applied Phycology, 2011Co-Authors: Héctor Mendoza Guzmán, Adelina Jara Valido, Laura Carmona Duarte, Karen Freijanes PresmanesAbstract:Relative polyunsaturated Fatty Acid content and unsaturation index are very important composition variables in the use of microalgae both for animal and human nutrition and biofuel production. A readily available technique to rapidly and inexpensively estimate relative Fatty Acid composition is very important for mass screening of new strains for the production of different types of oil. This study demonstrates the validity of Nile Red staining and flow cytometry for quick estimation of unsaturation index and relative Fatty Acid content in microalgae. Nile Red staining allows polar and neutral lipid contents to be estimated, and in this study a significant correlation was observed between polar/neutral ratio and Fatty Acid content in the species studied, corresponding to higher polyunsaturated Fatty Acid content in the polar lipid fraction of microalgae. This technique enables quick estimation of relative polyunsaturated Fatty Acid content and interspecific variation, as well as variations caused by culture conditions. In the species studied, most variability in Fatty Acid composition was due to variation in monounsaturated and polyunsaturated Fatty Acids, with less variation observed in saturated Fatty Acid content.
Arend Bonen - One of the best experts on this subject based on the ideXlab platform.
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Fatty Acid transport across the cell membrane: Regulation by Fatty Acid transporters
Prostaglandins Leukotrienes and Essential Fatty Acids, 2010Co-Authors: Robert W. Schwenk, Graham P. Holloway, Joost J. F. P. Luiken, Arend Bonen, Jan F. C. GlatzAbstract:Abstract Transport of long-chain Fatty Acids across the cell membrane has long been thought to occur by passive diffusion. However, in recent years there has been a fundamental shift in understanding, and it is now generally recognized that Fatty Acids cross the cell membrane via a protein-mediated mechanism. Membrane-associated Fatty Acid-binding proteins (‘Fatty Acid transporters') not only facilitate but also regulate cellular Fatty Acid uptake, for instance through their inducible rapid (and reversible) translocation from intracellular storage pools to the cell membrane. A number of Fatty Acid transporters have been identified, including CD36, plasma membrane-associated Fatty Acid-binding protein (FABP pm ), and a family of Fatty Acid transport proteins (FATP1–6). Fatty Acid transporters are also implicated in metabolic disease, such as insulin resistance and type-2 diabetes. In this report we briefly review current understanding of the mechanism of transmembrane Fatty Acid transport, and the function of Fatty Acid transporters in healthy cardiac and skeletal muscle, and in insulin resistance/type-2 diabetes. Fatty Acid transporters hold promise as a future target to rectify lipid fluxes in the body and regain metabolic homeostasis.
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rosiglitazone increases Fatty Acid oxidation and Fatty Acid translocase fat cd36 but not carnitine palmitoyltransferase i in rat muscle mitochondria
The Journal of Physiology, 2008Co-Authors: Carley R Benton, Graham P. Holloway, Joost J. F. P. Luiken, Jan F. C. Glatz, S E Campbell, Yuko Yoshida, Narendra N Tandon, Lawrence L Spriet, Arend BonenAbstract:Peroxisome proliferator-activated receptors (PPARs) alter the expression of genes involved in regulating lipid metabolism. Rosiglitazone, a PPARγ agonist, induces tissue-specific effects on lipid metabolism; however, its mode of action in skeletal muscle remains unclear. Since Fatty Acid translocase (FAT/CD36) was recently identified as a possible regulator of skeletal muscle Fatty Acid transport and mitochondrial Fatty Acid oxidation, we examined in this tissue the effects of rosiglitazone infusion (7 days, 1 mg day−1) on FAT/CD36 mRNA and protein, its plasmalemmal content and Fatty Acid transport. In addition, in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria we examined rates of Fatty Acid oxidation, FAT/CD36 and carnitine palmitoyltransferase I (CPTI) protein, and CPTI and β-hydroxyacyl CoA dehydrogenase (β-HAD) activities. Rosiglitazone did not alter FAT/CD36 mRNA or protein expression, FAT/CD36 plasmalemmal content, or the rate of Fatty Acid transport into muscle (P > 0.05). In contrast, rosiglitazone increased the rates of Fatty Acid oxidation in both SS (+21%) and IMF mitochondria (+36%). This was accompanied by concomitant increases in FAT/CD36 in subsarcolemmal (SS) (+43%) and intermyofibrillar (IMF) mitochondria (+46%), while SS and IMF CPTI protein content, and CPTI submaximal and maximal activities (P > 0.05) were not altered. Similarly, citrate synthase (CS) and β-HAD activities were also not altered by rosiglitazone in SS and IMF mitochondria (P > 0.05). These studies provide another example whereby changes in mitochondrial Fatty oxidation are associated with concomitant changes in mitochondrial FAT/CD36 independent of any changes in CPTI. Moreover, these studies identify for the first time a mechanism by which rosiglitazone stimulates Fatty Acid oxidation in skeletal muscle, namely the chronic, subcellular relocation of FAT/CD36 to mitochondria.
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exercise and insulin increase muscle Fatty Acid uptake by recruiting putative Fatty Acid transporters to the sarcolemma
Current Opinion in Clinical Nutrition and Metabolic Care, 2002Co-Authors: Jan F. C. Glatz, Arend Bonen, Joost J. F. P. LuikenAbstract:Purpose of review Skeletal muscle metabolic energy, needed to maintain contractile activity, is mainly obtained from glucose and long-chain Fatty Acids. Recent studies have revealed a remarkable parallel between the regulation of uptake of glucose and Fatty Acids by muscle, in that each is mediated by sarcolemmal transporters that are recruited from an intracellular storage site. The focus of this review is to describe newly obtained insights on the recruitment of Fatty Acid transporters and their malfunctioning in diabetes. Recent findings The major Fatty Acid transporter involved is Fatty Acid translocase (CD36). Translocation of this protein to the membrane is triggered by muscle contraction and by insulin, and presumably occurs from distinct intracellular pools. This resembles the well documented exercise and insulin-induced recruitment of glucose transporter-4. Whether another transporter, plasma membrane Fatty Acid-binding protein, is also subject to such recycling is not yet clear. In a rodent model of insulin-dependent (type 1) diabetes, the increased rate of muscle Fatty Acid uptake could be associated with an increased total amount of Fatty Acid translocase (CD36). In a model of non-insulin dependent (type 2) diabetes, this increased rate could be associated with a permanent relocalization of Fatty Acid translocase to the sarcolemma. Summary These findings indicate a pivotal role for the membrane transporter Fatty Acid translocase in the exercise and insulin-induced increases of muscle Fatty Acid uptake and utilization, and suggest that malfunctioning of the cellular recycling of Fatty Acid translocase is involved in the etiology of insulin resistance and type 2 diabetes.
