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Journal articles on the topic 'Acyl-CoAs metabolome'

Author: Grafiati

Published: 27 July 2024

Last updated: 31 July 2025

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1

Tokarska-Schlattner, Malgorzata, Nour Zeaiter, Valérie Cunin, et al. "Multi-Method Quantification of Acetyl-Coenzyme A and Further Acyl-Coenzyme A Species in Normal and Ischemic Rat Liver." International Journal of Molecular Sciences 24, no. 19 (2023): 14957. http://dx.doi.org/10.3390/ijms241914957.

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Thioesters of coenzyme A (CoA) carrying different acyl chains (acyl-CoAs) are central intermediates of many metabolic pathways and donor molecules for protein lysine acylation. Acyl-CoA species largely differ in terms of cellular concentrations and physico-chemical properties, rendering their analysis challenging. Here, we compare several approaches to quantify cellular acyl-CoA concentrations in normal and ischemic rat liver, using HPLC and LC-MS/MS for multi-acyl-CoA analysis, as well as NMR, fluorimetric and spectrophotometric techniques for the quantification of acetyl-CoAs. In particular,

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2

Brejchova, J., K. Brejchova, and O. Kuda. "Metabolic Pathways of Acylcarnitine Synthesis." Physiological Research, Suppl 1 (August 31, 2024): S153—S163. http://dx.doi.org/10.33549/physiolres.935261.

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Acylcarnitines are important markers in metabolic studies of many diseases, including metabolic, cardiovascular, and neurological disorders. We reviewed analytical methods for analyzing acylcarnitines with respect to the available molecular structural information, the technical limitations of legacy methods, and the potential of new mass spectrometry-based techniques to provide new information on metabolite structure. We summarized the nomenclature of acylcarnitines based on historical common names and common abbreviations, and we propose the use of systematic abbreviations derived from the sh

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3

Han, Lijuan, Ling Zhao, Yong Zhou, et al. "Altered metabolome and microbiome features provide clues in understanding irritable bowel syndrome and depression comorbidity." ISME Journal 16, no. 4 (2021): 983–96. http://dx.doi.org/10.1038/s41396-021-01123-5.

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AbstractIrritable bowel syndrome (IBS) is one of the functional gastrointestinal disorders characterized by chronic and/or recurrent symptoms of abdominal pain and irregular defecation. Changed gut microbiota has been proposed to mediate IBS; however, contradictory results exist, and IBS-specific microbiota, metabolites, and their interactions remain poorly understood. To address this issue, we performed metabolomic and metagenomic profiling of stool and serum samples based on discovery (n = 330) and validation (n = 101) cohorts. Fecal metagenomic data showed moderate dysbiosis compared with o

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4

IGAL, R. Ariel, Ping WANG, and Rosalind A. COLEMAN. "Triacsin C blocks de novo synthesis of glycerolipids and cholesterol esters but not recycling of fatty acid into phospholipid: evidence for functionally separate pools of acyl-CoA." Biochemical Journal 324, no. 2 (1997): 529–34. http://dx.doi.org/10.1042/bj3240529.

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The trafficking of acyl-CoAs within cells is poorly understood. In order to determine whether newly synthesized acyl-CoAs are equally available for the synthesis of all glycerolipids and cholesterol esters, we incubated human fibroblasts with [14C]oleate, [3H]arachidonate or [3H]glycerol in the presence or absence of triacsin C, a fungal metabolite that is a competitive inhibitor of acyl-CoA synthetase. Triacsin C inhibited de novo synthesis from glycerol of triacylglycerol, diacylglycerol and cholesterol esters by more than 93%, and the synthesis of phospholipid by 83%. However, the incorpora

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5

Pons, Roser, and Darryl C. De Vivo. "Primary and Secondary Carnitine Deficiency Syndromes." Journal of Child Neurology 10, no. 2_suppl (1995): 2S8–2S24. http://dx.doi.org/10.1177/0883073895010002s03.

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The objective of this article is to review primary and secondary causes of carnitine deficiency, emphasizing recent advances in our knowledge of fatty acid oxidation. It is now understood that the cellular metabolism of fatty acids requires the cytosolic carnitine cycle and the mitochondrial β-oxidation cycle. Carnitine is central to the translocation of the long chain acyl-CoAs across the inner mitochondrial membrane. The mitochondrial β-oxidation cycle is composed of a newly described membrane-bound system and the classic matrix compartment system. Very long chain acyl-CoA dehydrogenase and

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6

Yu, Wenfeng, Xiquan Liang, Regina E. Ensenauer, Jerry Vockley, Lawrence Sweetman та Horst Schulz. "Leaky β-Oxidation of atrans-Fatty Acid". Journal of Biological Chemistry 279, № 50 (2004): 52160–67. http://dx.doi.org/10.1074/jbc.m409640200.

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The degradation of elaidic acid (9-trans-octadecenoic acid), oleic acid, and stearic acid by rat mitochondria was studied to determine whether the presence of atransdouble bond in place of acisdouble bond or no double bond affects β-oxidation. Rat mitochondria from liver or heart effectively degraded the coenzyme A derivatives of all three fatty acids. However, with elaidoyl-CoA as a substrate, a major metabolite accumulated in the mitochondrial matrix. This metabolite was isolated and identified as 5-trans-tetradecenoyl-CoA. In contrast, little or none of the corresponding metabolites were de

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7

Varner, Erika L., Sophie Trefely, David Bartee, et al. "Quantification of lactoyl-CoA (lactyl-CoA) by liquid chromatography mass spectrometry in mammalian cells and tissues." Open Biology 10, no. 9 (2020): 200187. http://dx.doi.org/10.1098/rsob.200187.

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Lysine lactoylation is a recently described protein post-translational modification (PTM). However, the biochemical pathways responsible for this acylation remain unclear. Two metabolite-dependent mechanisms have been proposed: enzymatic histone lysine lactoylation derived from lactoyl-coenzyme A (lactoyl-CoA, also termed lactyl-CoA), and non-enzymatic lysine lactoylation resulting from acyl-transfer via lactoyl-glutathione. While the former has precedent in the form of enzyme-catalysed lysine acylation, the lactoyl-CoA metabolite has not been previously quantified in mammalian systems. Here,

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8

Xia, Chuanwu, Zhuji Fu, Kevin P. Battaile та Jung-Ja P. Kim. "Crystal structure of human mitochondrial trifunctional protein, a fatty acid β-oxidation metabolon". Proceedings of the National Academy of Sciences 116, № 13 (2019): 6069–74. http://dx.doi.org/10.1073/pnas.1816317116.

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Membrane-bound mitochondrial trifunctional protein (TFP) catalyzes β-oxidation of long chain fatty acyl-CoAs, employing 2-enoyl-CoA hydratase (ECH), 3-hydroxyl-CoA dehydrogenase (HAD), and 3-ketothiolase (KT) activities consecutively. Inherited deficiency of TFP is a recessive genetic disease, manifesting in hypoketotic hypoglycemia, cardiomyopathy, and sudden death. We have determined the crystal structure of human TFP at 3.6-Å resolution. The biological unit of the protein is α2β2. The overall structure of the heterotetramer is the same as that observed by cryo-EM methods. The two β-subunits

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9

Lone, Museer A., Andreas J. Hülsmeier, Essa M. Saied, et al. "Subunit composition of the mammalian serine-palmitoyltransferase defines the spectrum of straight and methyl-branched long-chain bases." Proceedings of the National Academy of Sciences 117, no. 27 (2020): 15591–98. http://dx.doi.org/10.1073/pnas.2002391117.

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Sphingolipids (SLs) are chemically diverse lipids that have important structural and signaling functions within mammalian cells. SLs are commonly defined by the presence of a long-chain base (LCB) that is normally formed by the conjugation ofl-serine and palmitoyl-CoA. This pyridoxal 5-phosphate (PLP)-dependent reaction is mediated by the enzyme serine-palmitoyltransferase (SPT). However, SPT can also metabolize other acyl-CoAs, in the range of C14to C18, forming a variety of LCBs that differ by structure and function. Mammalian SPT consists of three core subunits: SPTLC1, SPTLC2, and SPTLC3.

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10

Carrer, Alessandro, Joshua L. D. Parris, Sophie Trefely, et al. "Impact of a High-fat Diet on Tissue Acyl-CoA and Histone Acetylation Levels." Journal of Biological Chemistry 292, no. 8 (2017): 3312–22. http://dx.doi.org/10.1074/jbc.m116.750620.

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Cellular metabolism dynamically regulates the epigenome via availability of the metabolite substrates of chromatin-modifying enzymes. The impact of diet on the metabolism-epigenome axis is poorly understood but could alter gene expression and influence metabolic health. ATP citrate-lyase produces acetyl-CoA in the nucleus and cytosol and regulates histone acetylation levels in many cell types. Consumption of a high-fat diet (HFD) results in suppression of ATP citrate-lyase levels in tissues such as adipose and liver, but the impact of diet on acetyl-CoA and histone acetylation in these tissues

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11

Wu, Hao, Jingdan Liang, Lixia Gou, et al. "Recycling of Overactivated Acyls by a Type II Thioesterase during Calcimycin Biosynthesis in Streptomyces chartreusis NRRL 3882." Applied and Environmental Microbiology 84, no. 12 (2018): e00587-18. http://dx.doi.org/10.1128/aem.00587-18.

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ABSTRACT Type II thioesterases typically function as editing enzymes, removing acyl groups that have been misconjugated to acyl carrier proteins during polyketide secondary metabolite biosynthesis as a consequence of biosynthetic errors. Streptomyces chartreusis NRRL 3882 produces the pyrrole polyether ionophoric antibiotic, and we have identified the presence of a putative type II thioesterase-like sequence, calG, within the biosynthetic gene cluster involved in the antibiotic's synthesis. However, targeted gene mutagenesis experiments in which calG was inactivated in the organism did not lea

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12

Ozols, Juris. "Degradation of Hepatic Stearyl CoA Δ9-Desaturase". Molecular Biology of the Cell 8, № 11 (1997): 2281–90. http://dx.doi.org/10.1091/mbc.8.11.2281.

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Δ9-Desaturase is a key enzyme in the synthesis of desaturated fatty acyl-CoAs. Desaturase is an integral membrane protein induced in the endoplasmic reticulum by dietary manipulations and then rapidly degraded. The proteolytic machinery that specifically degrades desaturase and other short-lived proteins in the endoplasmic reticulum has not been identified. As the first step in identifying cellular factors involved in the degradation of desaturase, liver subcellular fractions of rats that had undergone induction of this enzyme were examined. In livers from induced animals, desaturase was prese

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13

Chen, Keting, Liza E. Alexander, Umnia Mahgoub, et al. "Dynamic relationships among pathways producing hydrocarbons and fatty acids of maize silk cuticular waxes." Plant Physiology, March 27, 2024. http://dx.doi.org/10.1093/plphys/kiae150.

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Abstract The hydrophobic cuticle is the first line of defense between aerial portions of plants and the external environment. On maize (Zea mays L.) silks, the cuticular cutin matrix is infused with cuticular waxes, consisting of a homologous series of very long-chain fatty acids (VLCFAs), aldehydes, and hydrocarbons. Together with VLC fatty-acyl-CoAs (VLCFA-CoAs), these metabolites serve as precursors, intermediates and end-products of the cuticular wax biosynthetic pathway. To deconvolute the potentially confounding impacts of the change in silk microenvironment and silk development on this

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14

Lee, Jennifer, Archana Vijayakumar, Phillip J. White, et al. "BCAA Supplementation in Mice with Diet-induced Obesity Alters the Metabolome Without Impairing Glucose Homeostasis." Endocrinology 162, no. 7 (2021). http://dx.doi.org/10.1210/endocr/bqab062.

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Abstract Circulating branched chain amino acid (BCAA) levels are elevated in obese humans and genetically obese rodents. However, the relationship of BCAAs to insulin resistance in diet-induced obese mice, a commonly used model to study glucose homeostasis, is still ill-defined. Here we examined how high-fat high-sucrose (HFHS) or high-fat diet (HFD) feeding, with or without BCAA supplementation in water, alters the metabolome in serum/plasma and tissues in mice and whether raising circulating BCAA levels worsens insulin resistance and glucose intolerance. Neither HFHS nor HFD feeding raised c

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15

Lee, Jennifer, Archana Vijayakumar, Phillip White, et al. "BCAA supplementation in mice with diet-induced obesity alters the metabolome without impairing glucose homeostasis." Endocrinology, July 2, 2021. https://doi.org/10.5061/dryad.fqz612jrt.

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Circulating branched chain amino acid (BCAA) levels are elevated in obese humans and genetically obese rodents. However, the relationship of BCAAs to insulin resistance in diet-induced obese mice, a commonly used model to study glucose homeostasis, is still ill-defined. Here we examined how high-fat high-sucrose (HFHS) or high-fat diet (HFD) feeding, with or without BCAA supplementation in water, alters the metabolome in serum/plasma and tissues in mice and whether raising circulating BCAA levels worsens insulin resistance and glucose intolerance. Neither HFHS nor HFD-feeding raised circulatin

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16

Tanosaki, Sho, Kenneth Bedi, Kenneth Margulies, and Zoltan Arany. "Abstract Tu113: Metabolomic Profile of Human End-Stage Ischemic Cardiomyopathy Reveals Few Differences from Non-Ischemic Cardiomyopathy." Circulation Research 135, Suppl_1 (2024). http://dx.doi.org/10.1161/res.135.suppl_1.tu113.

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Background: The heart is highly metabolic, relying on a range of fuels to sustain its high generation of ATP. The primary source of energy in the human heart is fatty acids, but fatty acid oxidation is reduced in failing hearts, contributing to a decrease in ATP production. Previously, we provided a comprehensive metabolic profile of human non-ischemic cardiomyopathy (NICM) hearts, including maintained ATP levels despite decreased energy charge (EC), lower acylcarnitines, acyl CoAs, and free fatty acids, suggesting a defect in fatty acid import. Research Questions: The pathogenesis of ischemic

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17

Meng, Yanting, Jianwen Ding, Yanping Wang, et al. "The transcriptional repressor Ctbp2 as a metabolite sensor regulating cardiomyocytes proliferation and heart regeneration." Molecular Medicine 31, no. 1 (2025). https://doi.org/10.1186/s10020-025-01168-8.

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Abstract Background C-terminal binding protein-2 (Ctbp2) is an evolutionarily conserved transcriptional repressor that regulates fundamental processes such as cell proliferation and apoptosis. However, the potential role of Ctbp2 in cardiomyocyte proliferation and heart regeneration remains unclear. In this study, we aim to explore the important role of Ctbp2 in cardiomyocyte proliferation and the regeneration of injured adult hearts. Methods and results In this study, we found that the expression of Ctbp2 in cardiomyocytes is downregulated after adulthood. Silencing Ctbp2 in cardiomyocytes on

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18

Sekiya, Motohiro, Kenta Kainoh, Takehito Sugasawa, et al. "The transcriptional corepressor CtBP2 serves as a metabolite sensor orchestrating hepatic glucose and lipid homeostasis." Nature Communications 12, no. 1 (2021). http://dx.doi.org/10.1038/s41467-021-26638-5.

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AbstractBiological systems to sense and respond to metabolic perturbations are critical for the maintenance of cellular homeostasis. Here we describe a hepatic system in this context orchestrated by the transcriptional corepressor C-terminal binding protein 2 (CtBP2) that harbors metabolite-sensing capabilities. The repressor activity of CtBP2 is reciprocally regulated by NADH and acyl-CoAs. CtBP2 represses Forkhead box O1 (FoxO1)-mediated hepatic gluconeogenesis directly as well as Sterol Regulatory Element-Binding Protein 1 (SREBP1)-mediated lipogenesis indirectly. The activity of CtBP2 is m

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19

SESHADRI, NIVEDITA, DEBORAH M. MUOIO, and ASHLEY S. WILLIAMS. "212-OR: Hepatic Overexpression of ACSS3 Alters Glucose Control and Fatty Acid Metabolism in Lean Mice." Diabetes 74, Supplement_1 (2025). https://doi.org/10.2337/db25-212-or.

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Introduction and Objective: Short chain fatty acids (SCFAs) are associated with adverse metabolic outcomes; however, little is known about their link to metabolic disease. Emerging evidence suggests that in addition to acting as signaling molecules, SCFAs also impact cellular metabolism via their conversion to acyl-CoAs by short chain acyl-CoA synthetase (ACSS) enzymes. ACSS3 is a mitochondrial enzyme highly expressed in liver; and recent studies from our laboratory using mass-spectrometry (MS)-based proteomics identified ACSS3 as the most downregulated protein in liver mitochondria from mice

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20

Ussher, John Edward R., Timothy R. Koves, Jagdip S. Jaswal, et al. "Abstract 5381: Insulin-Stimulated Glucose Oxidation is Increased in Hearts from High Fat Diet-Induced Obese Mice Lacking Malonyl CoA Decarboxylase." Circulation 118, suppl_18 (2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_539.

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OBJECTIVE - Diet-induced obesity (DIO) leads to an accumulation of intra-myocardial fatty acid metabolites that have been proposed to cause myocardial insulin resistance and dysfunction. Our goal was to determine the effect of DIO on myocardial fatty acid metabolite accumulation and how this is altered when mitochondrial fatty acid uptake is inhibited. This was achieved by using mice lacking malonyl CoA decarboxylase (MCD−/−), which have higher levels of malonyl CoA, an endogenous inhibitor of mitochondrial fatty acid uptake. METHODS - Wild type (WT) and MCD−/− mice were fed a low (4% kcal fro

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21

Dibble, Christian C., Samuel A. Barritt, Grace E. Perry, et al. "PI3K drives the de novo synthesis of coenzyme A from vitamin B5." Nature, July 27, 2022. http://dx.doi.org/10.1038/s41586-022-04984-8.

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AbstractIn response to hormones and growth factors, the class I phosphoinositide-3-kinase (PI3K) signalling network functions as a major regulator of metabolism and growth, governing cellular nutrient uptake, energy generation, reducing cofactor production and macromolecule biosynthesis1. Many of the driver mutations in cancer with the highest recurrence, including in receptor tyrosine kinases, Ras, PTEN and PI3K, pathologically activate PI3K signalling2,3. However, our understanding of the core metabolic program controlled by PI3K is almost certainly incomplete. Here, using mass-spectrometry-

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22

Nolen, Rayna M., Lene H. Petersen, Karl Kaiser, Antonietta Quigg, and David Hala. "In silico biomarker analysis of the adverse effects of perfluorooctane sulfonate (PFOS) exposure on the metabolic physiology of embryo-larval zebrafish." Frontiers in Systems Biology 4 (March 27, 2024). http://dx.doi.org/10.3389/fsysb.2024.1367562.

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Perfluorooctane sulfonate (PFOS) is a ubiquitous pollutant in global aquatic ecosystems with increasing concern for its toxicity to aquatic wildlife through inadvertent exposures. To assess the likely adverse effects of PFOS exposure on aquatic wildlife inhabiting polluted ecosystems, there is a need to identify biomarkers of its exposure and toxicity. We used an integrated systems toxicological framework to identify physiologically relevant biomarkers of PFOS toxicity in fish. An in silico stoichiometric metabolism model of zebrafish (Danio rerio) was used to integrate available (published by

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