Acute Regulation of Fatty Acid Uptake Involves the Cellular Redistribution of Fatty Acid Translocase

Bonen, Arend; Luiken, Joost J. F. P.; Arumugam, Y.; Glatz, Jan F. C.; Tandon, Narendra N.

doi:10.1074/jbc.275.19.14501

Cited by 320 publications

(386 citation statements)

References 51 publications

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“…In order to sustain the observed intracellular accumulation of LCPUFAs in brain cells, retrograde repartitioning is prevented by the binding of PUFAs to fatty acid binding proteins, followed by their rapid conversion to fatty acid coenzyme A (CoA) derivatives [36]. Kinetic studies of FA uptake by a variety of mammalian cell preparations revealed a saturable process with K m values in the nM range [36,[39][40][41]. This propensity to be saturated at low ligand concentrations necessarily limits intracellular concentrations of FAs.…”

Section: Discussionmentioning

confidence: 99%

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Richardson

Wurtman

2007

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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The synthesis of phospholipids in mammalian cells is regulated by the availability of three critical precursor pools: those of choline, cytidine triphosphate and diacylglycerol. Diacylglycerols containing polyunsaturated fatty acids (PUFAs) apparently are preferentially utilized for phosphatide synthesis. PUFAs are known to play an important role in the development and function of mammalian brains. We therefore studied the effects of unsaturated, monounsaturated and polyunsaturated fatty acids on the overall rates of phospholipid biosynthesis in PC12 rat pheochromocytoma cells. Docosahexaenoic acid (DHA, 22:6n-3), eicosapentaenoic acid (EPA, 20:5n-3) and arachidonic acid (AA, 20:4n-6) all significantly stimulated the incorporation of 14 C-choline into total cellular phospholipids. In contrast, monounsaturated oleic acid (OA) and the unsaturated palmitic (PA) and stearic (SA) acids did not have this effect. The action of DHA was concentration-dependent between 5 and 50 μM; it became statistically significant by 3 hrs after DHA treatment and then increased over the ensuing 3 hours. DHA was preferentially incorporated into phosphatidylethanolamine (PE) and phosphatidylserine (PS), while AA predominated in phosphatidylcholine (PC).

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Section: Discussionmentioning

confidence: 99%

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Richardson

Wurtman

2007

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…Permanent sarcolemmal FAT/CD36 relocation is dependent on obesity or type 2 diabetes Translocation of FAT/CD36 from intracellular depots to the sarcolemmal membrane of the muscle fibre is an important regulator of fatty acid transport and utilisation in muscle [31,32]. We monitored total FAT/CD36 levels by western blot on muscle tissue extracts from the four groups of donors (Fig.…”

Section: Participant Characteristicsmentioning

confidence: 99%

Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients

et al. 2010

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Aims/hypothesis Intramyocellular lipids (IMCL) accumulation is a classical feature of metabolic diseases. We hypothesised that IMCL accumulate mainly as a consequence of increased adiposity and independently of type 2 diabetes. To test this, we examined IMCL accumulation in two different models and four different populations of participants: muscle biopsies and primary human muscle cells derived from non-obese and obese participants with or without type 2 diabetes. The mechanism regulating IMCL accumulation was also studied. Methods Muscle biopsies were obtained from ten non-obese and seven obese participants without type 2 diabetes, and from eight non-obese and eight obese type 2 diabetic patients. Mitochondrial respiration, citrate synthase activity and both ON, Canada Diabetologia (2010) 53:1151-1163 DOI 10.1007/s00125-010-1708 accumulation is dependent upon obesity or type 2 diabetes and is related to sarcolemmal FAT/CD36 relocation. In cultured myotubes, IMCL content and FAT/CD36 relocation are independent of type 2 diabetes, suggesting that distinct factors in obesity and type 2 diabetes contribute to permanent FAT/CD36 relocation ex vivo.

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“…EVIDENCE SUGGESTS THAT MULTIPLE cellular signals regulate the changes in substrate metabolism with muscle contraction, including the AMP-activated protein kinase (AMPK) signaling cascade (2,34,35,52). During states of low energy, such as muscle contraction or exercise, it is widely accepted that liver kinase B1 (LKB1) acts as an upstream AMPK kinase that phosphorylates and activates AMPK and initiates a multitude of signaling events to maintain energy homeostasis (39 -41).…”

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confidence: 99%

AMPKα₂deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle

Abbott

Bogachus²,

Turcotte

2011

Journal of Applied Physiology

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Abbott MJ, Bogachus LD, Turcotte LP. AMPK␣2 deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle. J Appl Physiol 111: 125-134, 2011. First published May 5, 2011 doi:10.1152/japplphysiol.00807.2010.-AMP-activated protein kinase (AMPK) is a fuel sensor in skeletal muscle with multiple downstream signaling targets that may be triggered by increases in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]). The purpose of this study was to determine whether increases in intracellular [Ca 2ϩ ] induced by caffeine act solely via AMPK␣ 2 and whether AMPK␣2 is essential to increase glucose uptake, fatty acid (FA) uptake, and FA oxidation in contracting skeletal muscle. Hindlimbs from wild-type (WT) or AMPK␣ 2 dominant-negative (DN) transgene mice were perfused during rest (n ϭ 11), treatment with 3 mM caffeine (n ϭ 10), or muscle contraction (n ϭ 11). Time-dependent effects on glucose and FA uptake were uncovered throughout the 20-min muscle contraction perfusion period (P Ͻ 0.05). Glucose uptake rates did not increase in DN mice during muscle contraction until the last 5 min of the protocol (P Ͻ 0.05). FA uptake rates were elevated at the onset of muscle contraction and diminished by the end of the protocol in DN mice (P Ͻ 0.05). FA oxidation rates were abolished in the DN mice during muscle contraction (P Ͻ 0.05). The DN transgene had no effect on caffeine-induced FA uptake and oxidation (P Ͼ 0.05). Glucose uptake rates were blunted in caffeine-treated DN mice (P Ͻ 0.05). The DN transgene resulted in a greater use of intramuscular triglycerides as a fuel source during muscle contraction. The DN transgene did not alter caffeine-or contraction-mediated changes in the phosphorylation of Ca 2ϩ /calmodulin-dependent protein kinase I or ERK1/2 (P Ͼ 0.05). These data suggest that AMPK␣ 2 is involved in the regulation of substrate uptake in a time-dependent manner in contracting muscle but is not necessary for regulation of FA uptake and oxidation during caffeine treatment. ERK1/2; muscle contraction; caffeine; calcium/calmodulin-dependent protein kinase kinase; acetyl-CoA carboxylase EVIDENCE SUGGESTS THAT MULTIPLE cellular signals regulate the changes in substrate metabolism with muscle contraction, including the AMP-activated protein kinase (AMPK) signaling cascade (2, 34, 35, 52). During states of low energy, such as muscle contraction or exercise, it is widely accepted that liver kinase B1 (LKB1) acts as an upstream AMPK kinase that phosphorylates and activates AMPK and initiates a multitude of signaling events to maintain energy homeostasis (39 -41). Although strong evidence indicates that the LKB1-AMPK cascade is a key signaling pathway that regulates changes in glucose uptake, fatty acid (FA) uptake, and FA oxidation in contracting skeletal muscle (16,25,54,56), data also show that AMPK may not be the sole signal mediating contractioninduced changes in glucose uptake, FA uptake, and FA oxidation (35,36,56).Along with AMPK, mounting data suggest that increas...

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Acute Regulation of Fatty Acid Uptake Involves the Cellular Redistribution of Fatty Acid Translocase

Cited by 320 publications

References 51 publications

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients

AMPKα₂deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle

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Acute Regulation of Fatty Acid Uptake Involves the Cellular Redistribution of Fatty Acid Translocase

Cited by 320 publications

References 51 publications

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Polyunsaturated fatty acids stimulate phosphatidylcholine synthesis in PC12 cells

Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients

AMPKα2deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle

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AMPKα₂deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle