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Academic literature on the topic 'Acylcarnitines'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Acylcarnitines"

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Reuter, Stephanie E., Allan M. Evans, Randall J. Faull, Donald H. Chace, and Gianfranco Fornasini. "Impact of haemodialysis on individual endogenous plasma acylcarnitine concentrations in end-stage renal disease." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 42, no. 5 (September 1, 2005): 387–93. http://dx.doi.org/10.1258/0004563054889954.

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Background: Patients with end-stage renal disease (ESRD) undergoing long-term haemodialysis exhibit low L-carnitine and elevated acylcarnitine concentrations. This study evaluated endogenous concentrations of an array of acylcarnitines (carbon chain length up to 18) in healthy individuals and ESRD patients receiving haemodialysis, and examined the impact of a single haemodialysis session on acylcarnitine concentrations. Methods: Blood samples were collected from 60 healthy subjects and 50 ESRD patients undergoing haemodialysis (pre- and post-dialysis samples). Plasma samples were analysed for individual acylcarnitine concentrations by electrospray MS/MS. Results: Of the 31 acylcarnitines, 29 were significantly ( P<0.05) elevated in ESRD patients compared with healthy controls; in particular, C5 and C8:1 concentrations were substantially elevated. For acylcarnitines with a carbon chain length less than eight, plasma acylcarnitine concentrations decreased significantly over the course of a single dialysis session; however, post-dialysis concentrations invariably remained significantly higher than those in healthy subjects. Dialytic removal of acylcarnitines diminished once the acyl chain length exceeded eight carbons. Conclusions: The accumulation of acylcarnitines during long-term haemodialysis suggests that removal by haemodialysis is less efficient than removal from the body by the healthy kidney. Removal is significantly correlated to acyl chain length, most likely due to the increased molecular weight and lipophilicity that accompanies increased chain length.

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Guasch-Ferré, Marta, Miguel Ruiz-Canela, Jun Li, Yan Zheng, Mònica Bulló, Dong D. Wang, Estefanía Toledo, et al. "Plasma Acylcarnitines and Risk of Type 2 Diabetes in a Mediterranean Population at High Cardiovascular Risk." Journal of Clinical Endocrinology & Metabolism 104, no. 5 (November 13, 2018): 1508–19. http://dx.doi.org/10.1210/jc.2018-01000.

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Abstract Context The potential associations between acylcarnitine profiles and incidence of type 2 diabetes (T2D) and whether acylcarnitines can be used to improve diabetes prediction remain unclear. Objective To evaluate the associations between baseline and 1-year changes in acylcarnitines and their diabetes predictive ability beyond traditional risk factors. Design, Setting, and Participants We designed a case-cohort study within the PREDIMED Study including all incident cases of T2D (n = 251) and 694 randomly selected participants at baseline (follow-up, 3.8 years). Plasma acylcarnitines were measured using a targeted approach by liquid chromatography–tandem mass spectrometry. We tested the associations between baseline and 1-year changes in individual acylcarnitines and T2D risk using weighted Cox regression models. We used elastic net regressions to select acylcarnitines for T2D prediction and compute a weighted score using a cross-validation approach. Results An acylcarnitine profile, especially including short- and long-chain acylcarnitines, was significantly associated with a higher risk of T2D independent of traditional risk factors. The relative risks of T2D per SD increment of the predictive model scores were 4.03 (95% CI, 3.00 to 5.42; P < 0.001) for the conventional model and 4.85 (95% CI, 3.65 to 6.45; P < 0.001) for the model including acylcarnitines, with a hazard ratio of 1.33 (95% CI, 1.08 to 1.63; P < 0.001) attributed to the acylcarnitines. Including the acylcarnitines into the model did not significantly improve the area under the receiver operator characteristic curve (0.86 to 0.88, P = 0.61). A 1-year increase in C4OH-carnitine was associated with higher risk of T2D [per SD increment, 1.44 (1.03 to 2.01)]. Conclusions An acylcarnitine profile, mainly including short- and long-chain acylcarnitines, was significantly associated with higher T2D risk in participants at high cardiovascular risk. The inclusion of acylcarnitines into the model did not significantly improve the T2D prediction C-statistics beyond traditional risk factors, including fasting glucose.

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Li, Shangfu, Dan Gao, and Yuyang Jiang. "Function, Detection and Alteration of Acylcarnitine Metabolism in Hepatocellular Carcinoma." Metabolites 9, no. 2 (February 21, 2019): 36. http://dx.doi.org/10.3390/metabo9020036.

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Acylcarnitines play an essential role in regulating the balance of intracellular sugar and lipid metabolism. They serve as carriers to transport activated long-chain fatty acids into mitochondria for β-oxidation as a major source of energy for cell activities. The liver is the most important organ for endogenous carnitine synthesis and metabolism. Hepatocellular carcinoma (HCC), a primary malignancy of the live with poor prognosis, may strongly influence the level of acylcarnitines. In this paper, the function, detection and alteration of acylcarnitine metabolism in HCC were briefly reviewed. An overview was provided to introduce the metabolic roles of acylcarnitines involved in fatty acid β-oxidation. Then different analytical platforms and methodologies were also briefly summarised. The relationship between HCC and acylcarnitine metabolism was described. Many of the studies reported that short, medium and long-chain acylcarnitines were altered in HCC patients. These findings presented current evidence in support of acylcarnitines as new candidate biomarkers for studies on the pathogenesis and development of HCC. Finally we discussed the challenges and perspectives of exploiting acylcarnitine metabolism and its related metabolic pathways as a target for HCC diagnosis and prognosis.

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Dave, Amanda M., Thiago C. Genaro-Mattos, Zeljka Korade, and Eric S. Peeples. "Neonatal Hypoxic-Ischemic Brain Injury Alters Brain Acylcarnitine Levels in a Mouse Model." Metabolites 12, no. 5 (May 22, 2022): 467. http://dx.doi.org/10.3390/metabo12050467.

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Hypoxic-ischemic brain injury (HIBI) leads to depletion of ATP, mitochondrial dysfunction, and enhanced oxidant formation. Measurement of acylcarnitines may provide insight into mitochondrial dysfunction. Plasma acylcarnitine levels are altered in neonates after an HIBI, but individual acylcarnitine levels in the brain have not been evaluated. Additionally, it is unknown if plasma acylcarnitines reflect brain acylcarnitine changes. In this study, postnatal day 9 CD1 mouse pups were randomized to HIBI induced by carotid artery ligation, followed by 30 min at 8% oxygen, or to sham surgery and normoxia, with subgroups for tissue collection at 30 min, 24 h, or 72 h after injury (12 animals/group). Plasma, liver, muscle, and brain (dissected into the cortex, cerebellum, and striatum/thalamus) tissues were collected for acylcarnitine analysis by LC-MS. At 30 min after HIBI, acylcarnitine levels were significantly increased, but the differences resolved by 24 h. Palmitoylcarnitine was increased in the cortex, muscle, and plasma, and stearoylcarnitine in the cortex, striatum/thalamus, and cerebellum. Other acylcarnitines were elevated only in the muscle and plasma. In conclusion, although plasma acylcarnitine results in this study mimic those seen previously in humans, our data suggest that the plasma acylcarnitine profile was more reflective of muscle changes than brain changes. Acylcarnitine metabolism may be a target for therapeutic intervention after neonatal HIBI, though the lack of change after 30 min suggests a limited therapeutic window.

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Van Bocxlaer, J. F., and A. P. De Leenheer. "Solid-phase extraction technique for gas-chromatographic profiling of acylcarnitines." Clinical Chemistry 39, no. 9 (September 1, 1993): 1911–17. http://dx.doi.org/10.1093/clinchem/39.9.1911.

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Abstract We present a simple, new clean-up method for the gas-chromatographic profiling analysis of acylcarnitines. The use of a solid-phase, cation-exchange extraction combined with gas-chromatographic separation, based on the derivatization into acyloxylactones by Lowes and Rose (Analyst 1990;115:511-6), allows a selective and sensitive screening for acylcarnitines in urine. As such, a quantitative approach was developed for differential evaluation of acylcarnitines for detection of inborn errors of metabolism; the evaluation is both fast and routinely applicable in any biochemical laboratory. We validate the analysis method for acylcarnitines of various chain-lengths and present examples of its application to urine samples from diseased patients. We give special attention to the medium-chain acylcarnitines because of their association with medium-chain acylCoA dehydrogenase deficiency. Finally, the quantitative nature of the analysis allows evaluation of the acylcarnitine excretion over time.

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Schooneman, Marieke G., Niki Achterkamp, Carmen A. Argmann, Maarten R. Soeters, and Sander M. Houten. "Plasma acylcarnitines inadequately reflect tissue acylcarnitine metabolism." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1841, no. 7 (July 2014): 987–94. http://dx.doi.org/10.1016/j.bbalip.2014.04.001.

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An, Zhenni, Danmeng Zheng, Dongzhuo Wei, Dingwen Jiang, Xuejiao Xing, and Chang Liu. "Correlation between Acylcarnitine and Peripheral Neuropathy in Type 2 Diabetes Mellitus." Journal of Diabetes Research 2022 (February 17, 2022): 1–9. http://dx.doi.org/10.1155/2022/8115173.

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Objective. In patients with type 2 diabetes mellitus (T2DM), it is unknown whether acylcarnitine changes in the patient’s plasma as diabetic peripheral neuropathy (DPN) occurs. The purpose of the present study was to investigate the correlation between acylcarnitines and DPN in Chinese patients with T2DM. Methods. A total of 508 patients admitted to the First Affiliated Hospital of Jinzhou Medical University were included in this study, and all of whom were hospitalized for T2DM from January 2018 to December 2020. The diagnostic criteria for DPN were based on the 2017 Chinese Guidelines for the Prevention of Type 2 Diabetes. The contents of 25 acylcarnitine metabolites in fasting blood were determined by mass spectrometry. The measured acylcarnitines were classified by factor analysis, and the factors were extracted. To determine the correlation between acylcarnitines and DPN, binary logistic regression analysis was applied. Results. Among the 508 T2DM patients, 270 had DPN. Six factors were extracted from 25 acylcarnitines, and the cumulative contribution rate of variance was 61.02%. After the adjustment for other potential confounding factors, such as other carnitines and conventional risk factors, Factor 2 was positively associated with an increased risk of DPN (OR: 1.38, 95% CI: 1.13-1.69). Factor 2 contained acetylcarnitine (C2), propionylcarnitine (C3), butylcarnitine (C4), and isovalerylcarnitine (C5). Conclusions. Plasma levels of short-chain acylcarnitines (C2, C3, C4, and C5) were positively associated with DPN risk.

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Minkler, Paul E., Maria S. K. Stoll, Stephen T. Ingalls, Shuming Yang, Janos Kerner, and Charles L. Hoppel. "Quantification of Carnitine and Acylcarnitines in Biological Matrices by HPLC Electrospray Ionization– Mass Spectrometry." Clinical Chemistry 54, no. 9 (September 1, 2008): 1451–62. http://dx.doi.org/10.1373/clinchem.2007.099226.

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Abstract Background: Analysis of carnitine and acylcarnitines by tandem mass spectrometry (MS/MS) has limitations. First, preparation of butyl esters partially hydrolyzes acylcarnitines. Second, isobaric nonacylcarnitine compounds yield false-positive results in acylcarnitine tests. Third, acylcarnitine constitutional isomers cannot be distinguished. Methods: Carnitine and acylcarnitines were isolated by ion-exchange solid-phase extraction, derivatized with pentafluorophenacyl trifluoromethanesulfonate, separated by HPLC, and detected with an ion trap mass spectrometer. Carnitine was quantified with d3-carnitine as the internal standard. Acylcarnitines were quantified with 42 synthesized calibrators. The internal standards used were d6-acetyl-, d3-propionyl-, undecanoyl-, undecanedioyl-, and heptadecanoylcarnitine. Results: Example recoveries [mean (SD)] were 69.4% (3.9%) for total carnitine, 83.1% (5.9%) for free carnitine, 102.2% (9.8%) for acetylcarnitine, and 107.2% (8.9%) for palmitoylcarnitine. Example imprecision results [mean (SD)] within runs (n = 6) and between runs (n = 18) were, respectively: total carnitine, 58.0 (0.9) and 57.4 (1.7) μmol/L; free carnitine, 44.6 (1.5) and 44.3 (1.2) μmol/L; acetylcarnitine, 7.74 (0.51) and 7.85 (0.69) μmol/L; and palmitoylcarnitine, 0.12 (0.01) and 0.11 (0.02) μmol/L. Standard-addition slopes and linear regression coefficients were 1.00 and 0.9998, respectively, for total carnitine added to plasma, 0.99 and 0.9997 for free carnitine added to plasma, 1.04 and 0.9972 for octanoylcarnitine added to skeletal muscle, and 1.05 and 0.9913 for palmitoylcarnitine added to skeletal muscle. Reference intervals for plasma, urine, and skeletal muscle are provided. Conclusions: This method for analysis of carnitine and acylcarnitines overcomes the observed limitations of MS/MS methods.

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Rutkowsky, Jennifer M., Trina A. Knotts, Kikumi D. Ono-Moore, Colin S. McCoin, Shurong Huang, Dina Schneider, Shamsher Singh, Sean H. Adams, and Daniel H. Hwang. "Acylcarnitines activate proinflammatory signaling pathways." American Journal of Physiology-Endocrinology and Metabolism 306, no. 12 (June 15, 2014): E1378—E1387. http://dx.doi.org/10.1152/ajpendo.00656.2013.

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Incomplete β-oxidation of fatty acids in mitochondria is a feature of insulin resistance and type 2 diabetes mellitus (T2DM). Previous studies revealed that plasma concentrations of medium- and long-chain acylcarnitines (by-products of incomplete β-oxidation) are elevated in T2DM and insulin resistance. In a previous study, we reported that mixed d,l isomers of C12- or C14-carnitine induced an NF-κB-luciferase reporter gene in RAW 264.7 cells, suggesting potential activation of proinflammatory pathways. Here, we determined whether the physiologically relevant l-acylcarnitines activate classical proinflammatory signaling pathways and if these outcomes involve pattern recognition receptor (PRR)-associated pathways. Acylcarnitines induced the expression of cyclooxygenase-2 in a chain length-dependent manner in RAW 264.7 cells. l-C14 carnitine (5–25 μM), used as a representative acylcarnitine, stimulated the expression and secretion of proinflammatory cytokines in a dose-dependent manner. Furthermore, l-C14 carnitine induced phosphorylation of JNK and ERK, common downstream components of many proinflammatory signaling pathways including PRRs. Knockdown of MyD88, a key cofactor in PRR signaling and inflammation, blunted the proinflammatory effects of acylcarnitine. While these results point to potential involvement of PRRs, l-C14 carnitine promoted IL-8 secretion from human epithelial cells (HCT-116) lacking Toll-like receptors (TLR)2 and -4, and did not activate reporter constructs in TLR overexpression cell models. Thus, acylcarnitines have the potential to activate inflammation, but the specific molecular and tissue target(s) involved remain to be identified.

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Zhang, Ningning, Xiaopu Jia, Shuai Fan, Bin Wu, Shuqing Wang, and Bo OuYang. "NMR Characterization of Long-Chain Fatty Acylcarnitine Binding to the Mitochondrial Carnitine/Acylcarnitine Carrier." International Journal of Molecular Sciences 23, no. 9 (April 21, 2022): 4608. http://dx.doi.org/10.3390/ijms23094608.

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The mitochondrial carnitine/acylcarnitine carrier (CAC) transports short-, medium- and long-carbon chain acylcarnitines across the mitochondrial inner membrane in exchange for carnitine. How CAC recognizes the substrates with various fatty acyl groups, especially long-chain fatty acyl groups, remains unclear. Here, using nuclear magnetic resonance (NMR) technology, we have shown that the CAC protein reconstituted into a micelle system exhibits a typical six transmembrane structure of the mitochondrial carrier family. The chemical shift perturbation patterns of different fatty acylcarnitines suggested that the segment A76–G81 in CAC specifically responds to the long-chain fatty acylcarnitine. Molecular dynamics (MD) simulations of palmitoyl-L-carnitine inside the CAC channel showed the respective interaction and motion of the long-chain acylcarnitine in CAC at the cytosol-open state and matrix-open state. Our data provided a molecular-based understanding of CAC structure and transport mechanism.

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Dissertations / Theses on the topic "Acylcarnitines"

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Kelly, Barbara M. "The analysis of biological fluids for acylcarnitines." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326566.

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Ferro, Fabio. "Régulation des canaux ioniques cardiaques par les acylcarnitines." Thesis, Tours, 2012. http://www.theses.fr/2012TOUR3315/document.

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Plusieurs maladies entraînent soit une augmentation soit une diminution du taux des acides gras (AG) et de leurs dérivés circulants, notamment les acyl-carnitines (AC). Ce changement a été soupçonné comme étant la cause de importants dérangements électriques. Nous avons montré que les AC à chaine longue (LCAC) du côté extracellulaire modulent le canal hERG de façon spécifique, modulant sa amplitude de courant et sa cinétique. Aucun AC testé n’a eu d’effet en intracellulaire. La CAR et les MCAC n’ont eu aucun effet. Les AC ne modulent pas les courants IKS et IK1. Le canal Cav1.2 est modulé par C16-CAR et le C16 dans la lignée HEK293-ICaL et dans des cardiomyocytes de rat. En condition physiologique il existe donc un lien strict entre le métabolisme énergétique et activité électrique cardiaque qui entraine une modulation permanente du canal hERG par les LCAC. La régulation par les LCAC du canal hERG et peut être celle du canal ICaL, pourraient participer au dérangement électrique à l’origine du déclenchement de troubles du rythme cardiaque retrouvé dans certaines maladies
Several diseases can cause either an increase or a decrease in the rate of fatty acids (FAs) and their derivatives circulating, including acyl-carnitines (AC). This change is suspected as being the cause of major cardiac electrical perturbations. We have shown that long-chain AC (LCAC) modulate specifically by the extracellular side the hERG channel, regulating its current amplitude and kinetics. All AC tested had no effect when applied intracellularly. Carnitine and medium chain AC had no effect on hERG. LCAC does not modulate IK1 and IKS. Cav1.2 channel is modulated by C16 and C16-CAR in line HEK293-ICaL and rat cardiomyocytes. In physiological conditions there exists a strict link between energy metabolism and cardiac electrical activity which causes a permanent modulation of hERG channel by the LCAC. Regulation by the LCAC of the hERG channel and maybe ICaL, could participate in the electrical disturbance causing the onset of cardiac arrhythmia found in certain diseases

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Meadows, Jamie. "Carnitine and O-acylcarnitines in Pseudomonas aerguinosa: metabolism, transport, and regulation." ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/409.

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Pseudomonas aeruginosa is found in numerous environments and is an opportunistic pathogen affecting those who are immunocompromised. Its large genome encodes tremendous metabolic and regulatory diversity that enables P. aeruginosa to adapt to various environments. We are interested in how P. aeruginosa senses and responds to the host-derived compounds, carnitine and acylcarnitines. Acylcarnitines can be hydrolyzed to carnitine, where the liberated carnitine and its catabolic product glycine betaine can be used as osmoprotectants, for induction of the virulence factor phospholipase C, and as sole carbon, nitrogen, and energy sources. P. aeruginosa is incapable of de novo synthesis of carnitine and acylcarnitines and therefore imports these compounds from exogenous source. Short-chain acylcarnitines are imported by the ABC transporter CaiX-CbcWV. Medium- and long-chain acylcarnitines are hydrolyzed extracytoplasmically and the liberated carnitine is transported through CaiX-CbcWV. Once in the cytoplasm, short-chain acylcarnitines are hydrolyzed by the L-enantiomer specific hydrolase, HocS. The transcriptional regulator CdhR is divergently transcribed from the carnitine catabolism operon and we have identified the upstream activating region, the binding site sequence, and essential residues required for CdhR binding and induction of the carnitine operon. Carnitine catabolism is repressed by glucose and glycine betaine at the transcriptional level. Furthermore, using two different cdhR translational fusions we show that CdhR enhances its own expression and that GbdR, a related transcription factor, contributes to cdhR expression by enhancing the level of basal expression. These studies are the first to determine the mechanism of O-acylcarnitine transport, metabolism, and the regulation of these processes, which contribute to utilization of these compounds for P. aeruginosa survival in diverse environments.

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Angiletta, Chris. "The Role of Fasting Acylcarnitines in Metabolic Flexibility from Short Term High Fat Feeding." Thesis, Virginia Tech, 2018. http://hdl.handle.net/10919/82401.

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Metabolic flexibility plays a significant role in energy homeostasis by regulating fuel selection in correspondence to energy demand. Obese and type II diabetic populations have displayed a hindered ability to properly transition from fat oxidation while in a fasted state to carbohydrate oxidation once fed, leading to a buildup of mitochondrial metabolites such as acylcarnitines. Carnitine, essential for fatty acyl-CoA transport through the inner and outer mitochondrial membranes, can be an indicator of mitochondrial distress as elevated levels tend to spill over into plasma suggesting a disruption in oxidation. The current study was designed to examine the effect of short term, high fat feeding on plasma acylcarnitine species diversity and levels and if acylcarnitines are associated with metabolic flexibility. 13 healthy, non-obese, sedentary males, aged 18-40 years participated in this study. Following a 12-hour overnight fast a biopsy was taken from the quadricep before and 4 hours after a high fat meal. Blood draws were obtained pre-biopsy while fasted and every hour for 4 hours post high fat meal consumption. Acylcarnitines from plasma were converted to their butyl esters and analyzed by electrospray ionization tandem mass spectrometry (MS/MS). Changes were observed in acetylcarntine (P=0.0125), glucose oxidation (P=0.0295), C16:1/C16:0 desaturation index (P= 0.0397), and C18:1/C18:0 desaturation index (P=0.0012). We did not find that individual changes in flexibility correlated with circulating acylcarnitine measurements in a fasted state
Master of Science

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Lowes, Stephen. "Development of gas chromatography/mass spectrometry analysis of urinary acylcarnitines : application to metabolism studies." Thesis, Open University, 1991. http://oro.open.ac.uk/57333/.

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The metabolism of fatty acids in humans is recognized as an important source of energy. It is especially vital to newborn infants when metabolic pathways are often stressed as the early stages of life demand fundamental changes and developments of body processes. Defective fatty acid oxidation pathways can rapidly lead to a life-threatening situation. It has been suggested that such disorders may be responsible for a proportion of "cot death" or sudden infant death syndrome (SID S) cases. Recently, it has been found that the levels of acylcarnidnes in body fluids and tissue are potential indicators of fatty acid metabolism status. This is due to carnitine esters being produced and excreted in an attempt to alleviate the toxic accumulation of incompletely metabolized acyl units in the mitochondrion. However, clinical studies have been limited by a lack of convenient, unambiguous, sensitive and affordable analytical techniquesf or the measuremenot f physiological acylcarnitmnes. The nature of carnitine and its acyl esters presents analysis problems. They are involatile, zwitterionic compounds which makes them unsuitable for direct gas chromatography (GC) and combined gas chromatography/mass spectrometry (GCIMS). The latter of these is the favoured technique for normal urinary organic acid assays and is ideal in terms of selectivity and sensitivity. The work reported here details the development of a simple unambiguous and novel derivatization procedure in which acylcarnitines are cyclized to give volatile lactones, amenable to GC and GC/MS. The technique was subsequently applied to acylcarnitines extracted from urine. As such, the method has been used to identify acylcarnitine metabolites in the urine of children with diseases of fatty acid oxidation and amino acid catabolism. Investigations of the metabolism of exogenous 3-phenylpropionic and valproic acids was also conducted. The preliminary results from the application of capillary zone electrophoresis methods to acylcarnitine analysis are also reported.

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Brauer, Romy. "Einfluss präanalytischer Faktoren auf die Untersuchung des Aminosäure- und Acylcarnitinstoffwechsels." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-92011.

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Quantitative Untersuchungen krankheitsspezifischer oder krankheitsassoziierter metabolischer Signaturen in humanen Körperflüssigkeiten („Clinical Metabolomics“) haben zum Ziel neue Ansätze für diagnostische oder therapeutische Konzepte zu entwickeln. Die simultane quantitative Analytik von Aminosäuren (AS) und Acylcarnitinen (AC) mittels Tandem-Massenspektrometrie (MS/MS) ermöglicht die Erfassung wichtiger Stoffwechselwege des humanen Metabolismus. Hierzu zählen der Stoffwechsel der ketogenen AS, des Harnstoffzyklus oder der β-Oxidation langkettiger Fettsäuren. Allerdings wird die Konzentration der verschiedenen metabolischen Parameter in humanen Körperflüssigkeiten durch eine Vielzahl präanalytischer in vitro Störfaktoren und in vivo Einflussgrößen beeinflusst. Diese können zu signifikanten Veränderungen der Laborergebnisse führen. Im Rahmen meiner Promotionsarbeit wurden in vitro Störfaktoren (Probenmaterial, Lagerung u. a.) und in vivo Einflussgrößen (Ernährung, physische Aktivität) untersucht und ein standardisiertes Präanalytik-Protokoll entwickelt. Dazu wurden pro Probe 3 µL Trockenblut (TB), 10 µL Serum oder Plasma nach Butylierung mittels Elektrospray-Ionisations-MS/MS analysiert und jeweils 26 AS und 35 AC in 1,5 Minuten simultan bestimmt. Als Ergebnis der zahlreichen systematischen Präanalytik-Untersuchungen konnten signifikante Konzentrationsunterschiede der Metabolite zwischen kapillärer und venöser Blutentnahme sowie in Abhängigkeit des Hämatokrits gefunden werden. Im Vergleich zu Serum und antikoaguliertem Plasma (EDTA, Citrat, Heparin) waren die Konzentrationen der langkettigen AC im TB 5-fach höher. Nahrungsaufnahme und körperliche Aktivität führten ebenfalls zu signifikanten Veränderungen der AS- und AC-Konzentrationen. Durch Optimierung des Probenaufarbeitungsprotokolls konnte die Variabilität zwischen den Messtagen für 17 AS und 6 AC auf < 20 % gesenkt werden. Die Ergebnisse meiner Promotionsarbeit unterstreichen den Einfluss präanalytischer Faktoren auf die Metabolomanalytik. Durch Etablierung und Einhaltung standardisierter präanalytischer Protokolle kann die präanalytische Varianz der Ergebnisse deutlich verringert werden. Sie stellen somit eine wichtige Voraussetzung für eine qualitativ hochwertige Metabolomanalytik im Rahmen klinischer Studien zur Identifizierung neuer Biomarker dar.

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Van, Noolen Laetitia. "Syndrome d’apnées obstructives du sommeil et métabolisme lipidique : étude animale et étude clinique préliminaire." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAV035/document.

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Le syndrome d’apnées obstructives du sommeil (SAOS) est une pathologie caractérisée par des épisodes d’hypoxie intermittente (HI) nocturnes et est un problème de santé publique par sa prévalence dans la population générale (5-20%) et ses nombreuses complications métaboliques et cardiovasculaires. La répétition des épisodes d’HI est considérée comme le facteur principal responsable de cette morbidité cardiovasculaire dont l’athérosclérose fait partie. Le traitement de référence du SAOS par la pression positive continue présente dans certains cas une efficacité limitée, en particulier sur les conséquences cardiovasculaires qui nécessitent d’autres thérapeutiques plus spécifiques. Les mécanismes reliant SAOS et athérosclérose ne sont pas encore totalement connus. Cependant, des perturbations du métabolisme des acides gras (AG) en lien avec le processus athéromateux ont déjà été rapportées au cours du SAOS. Elles concernent en particulier le métabolisme de l’acide arachidonique (AG n-6) avec une augmentation d’eicosanoïdes pro-inflammatoires. Par ailleurs, les AG n-3 peuvent avoir une influence sur le développement et la progression des maladies cardiovasculaires, notamment grâce à une modification de la balance AG n-6 / AG n-3. Ainsi l’objectif de ce travail a donc été dans un premier temps de caractériser expérimentalement l’effet d’une supplémentation en AG n-3 sur le développement de l’athérosclérose dans le contexte d’HIC, et d’évaluer cliniquement la distribution AG n-6 / AG n-3 au niveau érythrocytaire chez des patients atteints d’un SAOS. Nous avons démontré que la supplémentation en AG n-3 permet de prévenir l’accélération de l’athérosclérose dans le contexte de l’HIC et est associée à une modulation de l’expression de certains médiateurs inflammatoires. Ces résultats prometteurs incitent à envisager une étude interventionnelle chez les patients SAOS. Dans un second temps, nous nous sommes intéressés au métabolisme des AG, via la β-oxydation mitochondriale, et aux métabolites intermédiaires produits, les acylcarnitines (ACs). Ces métabolites sont de plus en plus étudiés dans le contexte des pathologies cardiovasculaires. Nous avons étudié l’impact du SAOS sur la β-oxydation et ses conséquences sur la fonction vasculaire. L’étude de ces métabolites semble prometteuse et permettra peut-être l’émergence de marqueurs biologiques en relation avec l’état cardiovasculaire des patients
Obstructive sleep apnea (OSA) syndrome is a disease characterized by recurrent episodes of nocturnal intermittent hypoxia (IH). OSA is a major public health problem due to its frequency in general population (5 to 20%) and its numerous metabolic and cardiovascular complications. Repetitive apneas lead to IH which is responsible of early atherosclerosis and cardiovascular complications. Gold standard treatment of OSA, that is to say continuous positive airway pressure, has poor effects on OSA cardiovascular consequences in some patients, underlining the need of alternative therapeutic strategies. Underlying mechanisms linking OSA to atherosclerosis are still poorly understood. Nevertheless, a link between polyunsaturated fatty acids (PUFAs) metabolism changes and atheromatous process has already been report during OSA syndrome. Arachidonic acid (n-6 PUFA) metabolism leads to increased biosynthesis of pro-inflammatory eicosanoids during OSA. Moreover, n-3 PUFAs influence cardiovascular complications progression especially by modifying n-6 FA / n-3 FA balance. The aim of this work was first to evaluate the influence of n-3 PUFAs supplementation on a CIH induced atherosclerosis progression model, and to clinically evaluate erythrocyte n-6 PUFA / n-3 PUFA distribution in OSA patients. We have shown that n-3 PUFAs supplementation prevents atherosclerosis acceleration in CIH exposed mice and is associated with a modulation of inflammatory mediators. These promising results encourage us to consider an interventional clinical study in OSA patients. In a second time, we have studied FA mitochondrial β-oxidation metabolism via acylcarnitines (ACs) metabolites. These ACs are increasingly studied especially in cardiovascular diseases context. OSA impact on β-oxidation metabolism and its vascular function consequences have been evaluated. ACs study is promising and will perhaps allow biological markers emergence in relation to cardiovascular pattern

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Sim, Keow Giak. "Quantitative Fibroblast Acylcarnitine Profiling In The Diagnostic and Prognostic Assessment of Mitochondrial fatty acid [beta]-oxidation disorders." Thesis, The University of Sydney, 2002. http://hdl.handle.net/2123/801.

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Mitochondrial fatty acid ß-oxidation disorders are a group of clinically and biochemically heterogeneous defects mainly associated with intolerance to catabolic stress. The diseases are potentially fatal, but treatable and the prognosis for most diagnosed disorders is generally favourable. Early diagnosis is thus important to prevent morbidity and mortality. This project describes an improved and validated quantitative fibroblast acylcarnitine profile assay for the investigation of suspected fatty acid ß-oxidation disorders. Intact cells were incubated with deuterium-labelled hexadecanoate and L-carnitine, and the accumulated acylcarnitines in the medium analysed using electrospray tandem mass spectrometry. This modified procedure is less demanding technically, requires fewer cells and better reflects the in vivo acylcarnitine status than previously published methods. Mitochondrial fatty acid ß-oxidation is coupled to the respiratory chain. Functional defects of one pathway may lead to secondary alterations in flux through the other. The diagnostic specificity and the prognostic potential of the in vitro acylcarnitine profile assay were investigated in fibroblasts from 14 normal controls, 38 patients with eight enzyme deficiencies of fatty acid ß-oxidation presenting with various phenotypes, and 16 patients with primary respiratory chain defects including both isolated and multiple enzyme complex defects. All fatty acid ß-oxidation deficient cell lines revealed disease-specific acylcarnitine profiles related to the sites of defects irrespective of the severity of symptoms or of different mutation. Preliminary studies suggested a correlation between severity of symptoms and higher concentrations of long-chain acylcarnitine species. However, the fibroblast acylcarnitine profiles from some patients with respiratory chain defects were similar to those of controls, whereas others had abnormal profiles resembling those found in fatty acid ß-oxidation disorders. In vitro acylcarnitine profiling is useful for the detection of fatty acid ß-oxidation deficiencies, and perhaps the prediction of disease severity and prognostic evaluation facilitating decisions of therapeutic intervention and genetic counselling. However, abnormal profiles do not exclusively indicate these disorders, and primary defects of the respiratory chain remain a possibility. Awareness of this diagnostic pitfall will aid in the selection of subsequent confirmatory tests and therapeutic options.

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GRELLET, GREGORY. "Etude de sels d'ammonium quaternaire par spectrometrie de masse : application a la detection du profil des acylcarnitines dans le sang chez le nouveau-ne." Paris 6, 2000. http://www.theses.fr/2000PA066194.

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Le but de ce travail de these est la mise au point d'une methode de detection des esters methyliques d'acylcarnitines dans le sang, a l'aide du couplage entre la chromatographie liquide (h. P. L. C. ) et la spectrometrie de masse en tandem (triple quadripole). Cette methode nous a permis de diagnostiquer les erreurs du metabolisme du cycle de degradation des acides gras (-oxydation mitochondriale) et du cycle de degradation des acides amines a chaines ramifiees, chez le nouveau-ne. La mise au point de la methode passe par deux etapes. Tout d'abord on determine les ions permettant d'identifier chacun des composes recherches (ions diagnostics). Cette identification a ete deduite des schemas de fragmentations induites par collision avec l'argon de chacune des acylcarnitines et de chacun des esters methyliques correspondants. Parmi tous les fragments, le seul ion commun a toutes les acylcarnitines est l'ion m/z 85. Il est deplace a la masse m/z=99 pour les derives methyles. Une sensibilite plus grande est obtenue a partir des derives methyles. Ainsi, les profils seront etablis en recherchant les parents de leur ion diagnostic (m/z 99). La deuxieme etape consiste en la mise au point et la validation de l'extraction de nos produits a partir d'une goutte de sang deposee sur un papier filtre de type guthrie. Il a ete necessaire d'optimiser la nature du solvant et sa quantite. La derivation des acylcarnitines en esters methyliques d'acylcarnitines a egalement ete optimisee : nature du groupe protecteur, quantite, temps et temperature de reaction. A l'heure actuelle, ces tests ont ete effectues sur les prelevements de 200 patients et cette methode a ete validee pour 6 erreurs du metabolisme. Une application au dosage de l'octanoylcarnitine

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Sim, Keow Giak. "Quantitative Fibroblast Acylcarnitine Profiling In The Diagnostic and Prognostic Assessment of Mitochondrial Fatty Acid �-Oxidation Disorders." University of Sydney. Paediatrics and Child Health, 2002. http://hdl.handle.net/2123/801.

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Mitochondrial fatty acid �-oxidation disorders are a group of clinically and biochemically heterogeneous defects mainly associated with intolerance to catabolic stress. The diseases are potentially fatal, but treatable and the prognosis for most diagnosed disorders is generally favourable. Early diagnosis is thus important to prevent morbidity and mortality. This project describes an improved and validated quantitative fibroblast acylcarnitine profile assay for the investigation of suspected fatty acid �-oxidation disorders. Intact cells were incubated with deuterium-labelled hexadecanoate and L-carnitine, and the accumulated acylcarnitines in the medium analysed using electrospray tandem mass spectrometry. This modified procedure is less demanding technically, requires fewer cells and better reflects the in vivo acylcarnitine status than previously published methods. Mitochondrial fatty acid �-oxidation is coupled to the respiratory chain. Functional defects of one pathway may lead to secondary alterations in flux through the other. The diagnostic specificity and the prognostic potential of the in vitro acylcarnitine profile assay were investigated in fibroblasts from 14 normal controls, 38 patients with eight enzyme deficiencies of fatty acid �-oxidation presenting with various phenotypes, and 16 patients with primary respiratory chain defects including both isolated and multiple enzyme complex defects. All fatty acid �-oxidation deficient cell lines revealed disease-specific acylcarnitine profiles related to the sites of defects irrespective of the severity of symptoms or of different mutation. Preliminary studies suggested a correlation between severity of symptoms and higher concentrations of long-chain acylcarnitine species. However, the fibroblast acylcarnitine profiles from some patients with respiratory chain defects were similar to those of controls, whereas others had abnormal profiles resembling those found in fatty acid �-oxidation disorders. In vitro acylcarnitine profiling is useful for the detection of fatty acid �-oxidation deficiencies, and perhaps the prediction of disease severity and prognostic evaluation facilitating decisions of therapeutic intervention and genetic counselling. However, abnormal profiles do not exclusively indicate these disorders, and primary defects of the respiratory chain remain a possibility. Awareness of this diagnostic pitfall will aid in the selection of subsequent confirmatory tests and therapeutic options.

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Books on the topic "Acylcarnitines"

1

Parker, James N., and Philip M. Parker. Carnitine-acylcarnitine translocase deficiency: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. San Diego, CA: ICON Health Publications, 2007.

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Duran, Marinus, and Isabel Tavares de Almeida. Interpretation of Acylcarnitine Analysis Results. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0085.

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The analysis of acylcarnitines in plasma or blood spot samples by tandem mass spectrometry will detect all 15 defects of mitochondrial fatty acid beta-oxidation, although false negative results may occur in well-fed, non-fasting patients. Moreover, more than 20 organic acidemias can be detected by this methodological approach. An acylcarnitine profile should be part of the work-up of patients presenting with rhabdomyolysis and/or hypoglycemia and adults with an unexplained leukoencephalopathy. Cases with abnormal acylcarnitines require an analysis of urine organic acids as well as enzyme activity evaluation and molecular investigations to confirm the inherited defect.

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Belford, Michael William. The development of porous polymeric surfaces for screening acylcarnitines by laser desorption ionization mass spectrometry. 2003.

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Duran, Marinus, and Isabel Tavares de Almeida. Interpretation of Organic Acid Analysis Results. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0084.

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The analysis of organic acids in urine will detect more than 60 inherited conditions, most of which have clinical significance. Some of the abnormalities that are found represent non-diseases or artefacts of dietary/drug manipulations. Not all inherited organic acidemias are associated with excessively high excretion levels; some patients excrete the characteristic organic acids just above the upper normal level. This makes a quantitative analysis of organic acids a prerequisite. Approximately half of the organic acids will form acylcarnitines, therefore the analysis of carnitine and its esters is an important additional test.

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Murphy, Elaine, Yann Nadjar, and Christine Vianey-Saban. Fatty Acid Oxidation, Electron Transfer and Riboflavin Metabolism Defects. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0008.

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The fatty acid oxidation disorders are a group of autosomally recessively inherited disorders of energy metabolism that may present with life-threatening hypoketotic hypoglycemia, encephalopathy and hepatic dysfunction, muscle symptoms, and/or cardiomyopathy. Milder phenotypes may present in adulthood, causing exercise intolerance, episodic rhabdomyolysis, and neuropathy. Specific investigations include acylcarnitine profiling, urine organic acid analysis, fibroblast or leucocyte studies of fatty acid oxidation flux/enzyme activity, and genetic testing. Management varies depending on the condition but includes avoidance of precipitants such as fasting, fever, and intense exercise, a high-carbohydrate, low-fat diet, and supplementation with carnitine or riboflavin. Inborn errors of riboflavin transport mainly present with Brown-Vialetto-Van Laere syndrome. Some patients respond dramatically to riboflavin supplementation; therefore it has to be tried in all suspected patients.

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Book chapters on the topic "Acylcarnitines"

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Matern, Dietrich. "Acylcarnitines." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 775–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40337-8_51.

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Matern, Dietrich. "Acylcarnitines." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 65–74. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-67727-5_5.

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Beger, Richard D., Sudeepa Bhattacharyya, Pritmohinder S. Gill, and Laura P. James. "Acylcarnitines as Translational Biomarkers of Mitochondrial Dysfunction." In Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, 383–93. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119329725.ch24.

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Lepage, Nathalie, and Susan Aucoin. "Measurement of Plasma/Serum Acylcarnitines Using Tandem Mass Spectrometry." In Methods in Molecular Biology, 9–25. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-459-3_2.

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Millington, David S., and Donald H. Chace. "Carnitine and Acylcarnitines in Metabolic Disease Diagnosis and Management." In Mass Spectrometry, 299–318. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-1173-5_8.

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Duran, M., D. Ketting, L. Dorland, and S. K. Wadman. "The Identification of Acylcarnitines by Desorption Chemical Ionization Mass Spectrometry." In Inherited Disorders of Vitamins and Cofactors, 143–44. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-011-8019-1_44.

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Millington, David S., and Robert D. Stevens. "Acylcarnitines: Analysis in Plasma and Whole Blood Using Tandem Mass Spectrometry." In Methods in Molecular Biology, 55–72. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-61737-985-7_3.

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Corr, Peter B., J. E. Saffitz, and B. E. Sobel. "Lysophospholipids, long chain acylcarnitines and membrane dysfunction in the ischaemic heart." In Lipid metabolism in the normoxic and ischaemic heart, 199–208. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-08390-1_24.

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Vera, Nicholas B., Michelle Clasquin, Stephen L. Coy, and Paul Vouros. "The Use of DMS-MS for the Quantitative Analysis of Acylcarnitines." In Methods in Molecular Biology, 95–101. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0030-6_5.

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Sala, P. Ruiz, G. Ruijter, C. Acquaviva, A. Chabli, M. G. M. de Sain-van der Velden, J. Garcia-Villoria, M. R. Heiner-Fokkema, et al. "Pilot Experience with an External Quality Assurance Scheme for Acylcarnitines in Plasma/Serum." In JIMD Reports, 23–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_533.

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Conference papers on the topic "Acylcarnitines"

1

Shen, Eric Yi-Liang, Abellona U, Simon Taylor-Robinson, Mark Thursz, Elaine Holmes, and Jeremy Nicholson. "Abstract 5269: Discovery and validation of plasma acylcarnitines for the early diagnosis of hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5269.

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Shen, Eric Yi-Liang, Abellona U, Simon Taylor-Robinson, Mark Thursz, Elaine Holmes, and Jeremy Nicholson. "Abstract 5269: Discovery and validation of plasma acylcarnitines for the early diagnosis of hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5269.

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Sulaj, A., S. Kopf, T. Fleming, A. Teleman, J. Okun, J. Szendrödi, S. Herzig, and P. Nawroth. "Intermittent fasting has short-term effects on albuminuria, AGE formation and acylcarnitines in patients with type 2 diabetes mellitus." In Late Breaking Abstracts Diabetes Kongress 2021 – 55. Jahrestagung der DDG Präzisionsmedizin – Eine Reise in die Zukunft der Diabetologie www.diabeteskongress.de. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730863.

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Junior, Rubens Paula, Nathália Martins Sonehara, and Debora A. P. C. Zuccari. "Abstract B85: Plasmatic levels of arginine, its precursors and acylcarnitines affected by melatonin at specific time of the day." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-b85.

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Zuccari, Debora, Rubens Paula Junior, Nathália Martins Sonehara, Roger Chammas, and Florence Raynaud. "Abstract 2504: Melatonin decreases plasma arginine, its precursors and acylcarnitines in breast cancer xenograft model at specific time point during circadian rhythm." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2504.

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"Amino acid and acylcarnitine levels relate with chronic schizophrenia." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-295.

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Gonzalez-Granda, A., A. Damms-Machado, M. Basrai, and C. Stephan. "Changes in Plasma Acylcarnitine and Lysophosphatidylcholine Levels Following a High-Fructose Diet: A Targeted Metabolomics Study in Healthy Women." In Ernährung – „Gewissheit“ im Fluss! Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1684902.

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