Relevant bibliographies by topics / Acyl-CoA analog

Academic literature on the topic 'Acyl-CoA analog'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Acyl-CoA analog"

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Lahiri, Sujoy, Hyejung Park, Elad L. Laviad, Xuequan Lu, Robert Bittman, and Anthony H. Futerman. "Ceramide Synthesis Is Modulated by the Sphingosine Analog FTY720 via a Mixture of Uncompetitive and Noncompetitive Inhibition in an Acyl-CoA Chain Length-de pend ent Manner." Journal of Biological Chemistry 284, no. 24 (April 8, 2009): 16090–98. http://dx.doi.org/10.1074/jbc.m807438200.

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FTY720, a sphingosine analog, is in clinical trials as an immunomodulator. The biological effects of FTY720 are believed to occur after its metabolism to FTY720 phosphate. However, very little is known about whether FTY720 can interact with and modulate the activity of other enzymes of sphingolipid metabolism. We examined the ability of FTY720 to modulate de novo ceramide synthesis. In mammals, ceramide is synthesized by a family of six ceramide synthases, each of which utilizes a restricted subset of acyl-CoAs. We show that FTY720 inhibits ceramide synthase activity in vitro by noncompetitive inhibition toward acyl-CoA and uncompetitive inhibition toward sphinganine; surprisingly, the efficacy of inhibition depends on the acyl-CoA chain length. In cultured cells, FTY720 has a more complex effect, with ceramide synthesis inhibited at high (500 nm to 5 μm) but not low (<200 nm) sphinganine concentrations, consistent with FTY720 acting as an uncompetitive inhibitor toward sphinganine. Finally, electrospray ionization-tandem mass spectrometry demonstrated, unexpectedly, elevated levels of ceramide, sphingomyelin, and hexosylceramides after incubation with FTY720. Our data suggest a novel mechanism by which FTY720 might mediate some of its biological effects, which may be of mechanistic significance for understanding its mode of action.
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Mells, Jamie E., Ping P. Fu, Shvetank Sharma, Darin Olson, Lihong Cheng, Jeffrey A. Handy, Neeraj K. Saxena, Dan Sorescu, and Frank A. Anania. "Glp-1 analog, liraglutide, ameliorates hepatic steatosis and cardiac hypertrophy in C57BL/6J mice fed a Western diet." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 2 (January 2012): G225—G235. http://dx.doi.org/10.1152/ajpgi.00274.2011.

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The aims of this study were designed to determine whether liraglutide, a long-acting glucagon-like peptide, could reverse the adverse effects of a diet high in fat that also contained trans-fat and high-fructose corn syrup (ALIOS diet). Specifically, we examined whether treatment with liraglutide could reduce hepatic insulin resistance and steatosis as well as improve cardiac function. Male C57BL/6J mice were pair fed or fed ad libitum either standard chow or the ALIOS diet. After 8 wk the mice were further subdivided and received daily injections of either liraglutide or saline for 4 wk. Hyperinsulinemic-euglycemic clamp studies were performed after 6 wk, revealing hepatic insulin resistance. Glucose tolerance and insulin resistance tests were performed at 8 and 12 wk prior to and following liraglutide treatment. Liver pathology, cardiac measurements, blood chemistry, and RNA and protein analyses were performed. Clamp studies revealed hepatic insulin resistance after 6 wk of ALIOS diet. Liraglutide reduced visceral adiposity and liver weight ( P < 0.001). As expected, liraglutide improved glucose and insulin tolerance. Liraglutide improved hypertension ( P < 0.05) and reduced cardiac hypertrophy. Surprisingly, liver from liraglutide-treated mice had significantly higher levels of fatty acid binding protein, acyl-CoA oxidase II, very long-chain acyl-CoA dehydrogenase, and microsomal triglyceride transfer protein. We conclude that liraglutide reduces the harmful effects of an ALIOS diet by improving insulin sensitivity and by reducing lipid accumulation in liver through multiple mechanisms including, transport, and increase β-oxidation.
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Satoh, A. "Structure of the Transition State Analog of Medium-Chain Acyl-CoA Dehydrogenase. Crystallographic and Molecular Orbital Studies on the Charge-Transfer Complex of Medium-Chain Acyl-CoA Dehydrogenase with 3-Thiaoctanoyl-CoA." Journal of Biochemistry 134, no. 2 (August 1, 2003): 297–304. http://dx.doi.org/10.1093/jb/mvg143.

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Wang, Yutong, and John F. Oram. "Unsaturated Fatty Acids Phosphorylate and Destabilize ABCA1 through a Phospholipase D2 Pathway." Journal of Biological Chemistry 280, no. 43 (August 23, 2005): 35896–903. http://dx.doi.org/10.1074/jbc.m506210200.

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Abnormal high density lipoprotein (HDL) metabolism among patients with diabetes and insulin resistance may contribute to their increased risk of atherosclerosis. ATP-binding cassette transporter ABCA1 mediates the transport of cholesterol and phospholipids from cells to HDL apolipoproteins and thus modulates HDL levels and atherogenesis. Unsaturated fatty acids, which are elevated in diabetes, impair the ABCA1 pathway in cultured cells by destabilizing ABCA1 protein. Here we examined the cellular pathway that mediates the ABCA1 destabilizing effects of fatty acids. The long-chain acyl-CoA synthetase inhibitor triacsin C completely reversed fatty acid-induced ABCA1 destabilization, indicating that fatty acids need to be activated to their CoA derivatives to enhance ABCA1 degradation. Unsaturated but not saturated fatty acids stimulated phospholipase D (PLD) activity, the PLD inhibitor 1-butanol prevented the unsaturated fatty acid-induced reduction in ABCA1 levels, and the PLD2 activator mastoparan markedly reduced ABCA1 protein levels, implicating a role for PLD2 in the ABCA1 destabilizing effects of fatty acids. Unsaturated fatty acids and mastoparan increased phosphorylation of ABCA1 serines. PLD2 small interfering RNA abolished the ability of unsaturated fatty acids to inhibit lipid transport activity, to reduce protein levels, and to increase serine phosphorylation of ABCA1. The diacylglycerol analog oleoylacetylglycerol also reduced ABCA1 protein levels and increased its serine phosphorylation, suggesting that PLD2-generated diacylglycerols promote the destabilizing phosphorylation of ABCA1. These data provide evidence that intracellular unsaturated acyl-CoA derivatives destabilize ABCA1 by activating a PLD2 signaling pathway.
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Shockey, J. M., R. Rajasekharan, and J. D. Kemp. "Photoaffinity Labeling of Developing Jojoba Seed Microsomal Membranes with a Photoreactive Analog of Acyl-Coenzyme A (Acyl-CoA) (Identification of a Putative Acyl-CoA:Fatty Alcohol Acyltransferase." Plant Physiology 107, no. 1 (January 1, 1995): 155–60. http://dx.doi.org/10.1104/pp.107.1.155.

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Nishina, Y. "Molecular Mechanism of the Drop in the pKa of a Substrate Analog Bound to Medium-Chain Acyl-CoA Dehydrogenase: Implications for Substrate Activation." Journal of Biochemistry 134, no. 6 (December 1, 2003): 835–42. http://dx.doi.org/10.1093/jb/mvg209.

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van Loon, Luc J. C., Michaela Thomason-Hughes, Dumitru Constantin-Teodosiu, René Koopman, Paul L. Greenhaff, D. Grahame Hardie, Hans A. Keizer, Wim H. M. Saris, and Anton J. M. Wagenmakers. "Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans." American Journal of Physiology-Endocrinology and Metabolism 289, no. 3 (September 2005): E482—E493. http://dx.doi.org/10.1152/ajpendo.00092.2005.

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This study investigates the consequences of inhibition of adipose tissue lipolysis on skeletal muscle substrate use. Ten subjects were studied at rest and during exercise and subsequent recovery under normal, fasting conditions (control trial, CON) and following administration of a nicotinic acid analog (low plasma free fatty acid trial, LFA). Continuous [U-13C]palmitate and [6,6-2H2]glucose infusions were applied to quantify plasma free fatty acid (FFA) and glucose oxidation rates and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected to measure 1) fiber type-specific IMTG content; 2) allosteric regulators of hormone-sensitive lipase (HSL), glycogen phosphorylase, and pyruvate dehydrogenase; and 3) the phosphorylation status of HSL at Ser563 and Ser565. Administration of a nicotinic acid analog (acipimox) substantially reduced plasma FFA rate of appearance and subsequent plasma FFA concentrations ( P < 0.0001). At rest, this substantially reduced plasma FFA oxidation rates, which was compensated by an increase in the estimated IMTG use ( P < 0.05). During exercise, the progressive increase in FFA rate of appearance, uptake, and oxidation was prevented in the LFA trial and matched by greater IMTG and glycogen use. Differential phosphorylation of HSL or relief of its allosteric inhibition by long-chain fatty acyl-CoA could not explain the increase in muscle TG use, but there was evidence to support the contention that regulation may reside at the level of the glucose-fatty acid cycle. This study confirms the hypothesis that plasma FFA availability regulates both intramuscular lipid and glycogen use in vivo in humans.
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Heller, R., F. Bussolino, D. Ghigo, G. Garbarino, G. Pescarmona, U. Till, and A. Bosia. "Human endothelial cells are target for platelet-activating factor. II. Platelet-activating factor induces platelet-activating factor synthesis in human umbilical vein endothelial cells." Journal of Immunology 149, no. 11 (December 1, 1992): 3682–88. http://dx.doi.org/10.4049/jimmunol.149.11.3682.

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Abstract Platelet-activating factor (PAF), a phospholipid mediator with broad and potent biologic activities, is synthesized by several inflammatory cells including endothelial cells (EC). PAF is also an effective stimulating agent for EC leading to increased cell permeability and adhesivity. We examined the synthesis of PAF in human umbilical cord vein EC after stimulation of EC with PAF or with its nonmetabolizable analog 1-O-alkyl-2-N-methyl-carbamyl-sn-glycero-3-phosphocholine (C-PAF). PAF (1 to 100 nM) induced a dose- and time-dependent increase of PAF synthesis as detected by [3H]acetate incorporation into PAF fraction. Stimulation of PAF synthesis occurred via activation of the "remodeling pathway" as the 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine (lyso-PAF):acetyl-CoA acetyltransferase was dose-dependently increased after PAF treatment. The de novo pathway of PAF synthesis was not activated under these conditions. C-PAF was able to mimic the effect of authentic PAF on [3H] acetate incorporation. The inactive metabolite lyso-PAF (100 nM) had no influence on PAF synthesis in EC. CV-3988, BN 52021, and WEB 2086, potent and specific antagonists of PAF suppressed PAF effects on the remodeling pathway completely. The PAF- and C-PAF-induced [3H]PAF remained 93% cell-associated and was not degraded up to 10 min after stimulation. Characterization of the [3H]acetate-labeled material co-migrating with authentic PAF revealed that a significant proportion (approximately 57%) was actually 1-acyl-2-acetyl-sn-glycero-3-phosphocholine. PAF-induced PAF synthesis might be an important mechanism for amplifying original PAF signals and potentiating adhesive interactions of circulating cells with the endothelium.
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THORPE, Colin, Thomas L. CIARDELLI, Charles J. STEWART, and Theodor WIELAND. "Interaction of Long-Chain Acyl-CoA Analogs with Pig Kidney General Acyl-CoA Dehydrogenase." European Journal of Biochemistry 118, no. 2 (March 3, 2005): 279–82. http://dx.doi.org/10.1111/j.1432-1033.1981.tb06397.x.

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Costa, Catarina G., Lambertus Dorland, Ulbe Holwerda, Isabel Tavares de Almeida, Bwee-Tien Poll-The, Cornelis Jakobs, and Marinus Duran. "Simultaneous analysis of plasma free fatty acids and their 3-hydroxy analogs in fatty acid β-oxidation disorders." Clinical Chemistry 44, no. 3 (March 1, 1998): 463–71. http://dx.doi.org/10.1093/clinchem/44.3.463.

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Abstract We present a new derivatization procedure for the simultaneous gas chromatographic–mass spectrometric analysis of free fatty acids and 3-hydroxyfatty acids in plasma. Derivatization of target compounds involved trifluoroacetylation of hydroxyl groups and tert-butyldimethylsilylation of the carboxyl groups. This new derivatization procedure had the advantage of allowing the complete baseline separation of free fatty acids and 3-hydroxyfatty acids while the superior gas chromatographic and mass spectrometric properties of tert-butyldimethylsilyl derivatives remained unchanged, permitting a sensitive analysis of the target compounds. Thirty-nine plasma samples from control subjects and patients with known defects of mitochondrial fatty acid β-oxidation were analyzed. A characteristic increase of long-chain 3-hydroxyfatty acids was observed for all of the long-chain 3-hydroxyacyl-CoA dehydrogenase-deficient and mitochondrial trifunctional protein-deficient plasma samples. For medium-chain acyl-CoA dehydrogenase deficiency and very-long-chain acyl-CoA dehydrogenase deficiency, decenoic and tetradecenoic acids, respectively, were the main abnormal fatty acids, whereas the multiple acyl-CoA dehydrogenase-deficient patients showed variable increases of these unusual intermediates. The results showed that this selective and sensitive method is a powerful tool in the diagnosis and monitoring of mitochondrial fatty acid β-oxidation disorders.
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Dissertations / Theses on the topic "Acyl-CoA analog"

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Lamm, Teresa Renée. "Redox modulation of acyl-CoA dehydrogenases (ACDs) and their ligands in several ACD-analog systems /." Diss., ON-CAMPUS Access For University of Minnesota, Twin Cities Click on "Connect to Digital Dissertations", 2001. http://www.lib.umn.edu/articles/proquest.phtml.

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Book chapters on the topic "Acyl-CoA analog"

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Shockey, Jay M., John D. Kemp, and Ram Rajasekharan. "Identification of Jojoba Seed acyl-CoA:Fatty Alcohol Acyltransferase by Photolabeling with acyl-CoA Analog." In Plant Lipid Metabolism, 540–42. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_150.

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