Journal articles: 'Short chain acylcarnitine'

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Hiatt, W. R., D. Nawaz, and E. P. Brass. "Carnitine metabolism during exercise in patients with peripheral vascular disease." Journal of Applied Physiology 62, no. 6 (June 1, 1987): 2383–87. http://dx.doi.org/10.1152/jappl.1987.62.6.2383.

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The distribution between carnitine and the acyl derivatives of carnitine reflects changes in the metabolic state of a variety of tissues. Patients with peripheral vascular disease (PVD) develop skeletal muscle ischemia with exertion. This impairment in oxidative metabolism during exercise may result in the generation of acylcarnitines. To test this hypothesis, 11 patients with PVD and 7 age-matched control subjects were evaluated with graded treadmill exercise. Subjects with PVD walked to maximal claudication pain at a peak O2 consumption (VO2) of 19.9 +/- 1.3 ml X kg-1 X min-1 (mean +/- SE). Control subjects were taken to a near-maximal work load at a VO2 of 31.3 +/- 1.0 ml X kg-1 X min-1. In patients with PVD, the plasma concentration of total acid-soluble, long-chain acylcarnitine and total carnitine was increased at peak exercise compared with resting values. Four minutes postexercise, the plasma short-chain acylcarnitine concentration was also increased. In control subjects taken to the higher work load, only the long-chain acylcarnitine concentration was increased at peak exercise. In patients with PVD, plasma short-chain acylcarnitine concentration at rest was negatively correlated with subsequent maximal walking time (r = -0.51, P less than 0.05). In conclusion, acylcarnitines increased in patients with PVD who walked to maximal claudication pain, whereas control subjects did not show equivalent changes even when taken to a higher work load. The relationship between short-chain acylcarnitine concentration at rest and subsequent exercise performance suggests that repeated episodes of ischemia may cause chronic accumulation of short-chain acylcarnitine in plasma in proportion to the severity of disease.(ABSTRACT TRUNCATED AT 250 WORDS)

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Meadows, Jamie A., and Matthew J. Wargo. "Characterization of Pseudomonas aeruginosa Growth onO-Acylcarnitines and Identification of a Short-Chain Acylcarnitine Hydrolase." Applied and Environmental Microbiology 79, no. 11 (March 22, 2013): 3355–63. http://dx.doi.org/10.1128/aem.03943-12.

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ABSTRACTTo survive in various environments, from host tissue to soil, opportunistic bacterial pathogens must be metabolically flexible and able to use a variety of nutrient sources. We are interested inPseudomonas aeruginosa's catabolism of quaternary amine compounds that are prevalent in association with eukaryotes. Carnitine and acylcarnitines are abundant in animal tissues, particularly skeletal muscle, and are used to shuttle fatty acids in and out of the mitochondria, where they undergo β-oxidation. We previously identified the genes required for carnitine catabolism as the first four genes in the carnitine operon (caiX-cdhCAB;PA5388toPA5385). However, the last gene in the operon,PA5384, was not required for carnitine catabolism. We were interested in determining the function of PA5384. Bioinformatic analyses along with the genomic location ofPA5384led us to hypothesize a role for PA5384 in acylcarnitine catabolism. Here, we have characterized PA5384 as anl-enantiomer-specific short-chain acylcarnitine hydrolase that is required for growth and hydrolysis of acetyl- and butyrylcarnitine to carnitine and the respective short-chain fatty acid. The liberated carnitine and its downstream catabolic product, glycine betaine, are subsequently available to function as osmoprotectants in hyperosmotic environments and induce transcription of the virulence factor phospholipase C,plcH. Furthermore, we confirmed that acylcarnitines with 2- to 16-carbon chain lengths, except for octanoylcarnitine (8 carbons), can be utilized byP. aeruginosaas sole carbon and nitrogen sources. These findings expand our knowledge of short-chain acylcarnitine catabolism and also point to remaining questions related to acylcarnitine transport and hydrolysis of medium- and long-chain acylcarnitines.

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Hiatt, W. R., E. E. Wolfel, J. G. Regensteiner, and E. P. Brass. "Skeletal muscle carnitine metabolism in patients with unilateral peripheral arterial disease." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 346–53. http://dx.doi.org/10.1152/jappl.1992.73.1.346.

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Patients with peripheral arterial disease (PAD) have abnormalities of carnitine metabolism that may contribute to their functional impairment. To test the hypothesis that muscle acylcarnitine generation (intermediates in oxidative metabolism) in patients with PAD provides a marker of the muscle dysfunction, 10 patients with unilateral PAD and 6 age-matched control subjects were studied at rest, and the patients were studied during exercise. At rest, biopsies of the gastrocnemius muscle in the patients' nonsymptomatic leg revealed a normal carnitine pool and lactate content compared with control subjects. In contrast, the patients' diseased leg had higher contents of lactate and long-chain acylcarnitines than controls. The muscle short-chain acylcarnitine content in the patients' diseased leg at rest was inversely correlated with peak exercise performance (r = -0.75, P less than 0.05). With graded treadmill exercise, only patients who exceeded their individual lactate threshold had an increase in muscle short-chain acylcarnitine content in the nonsymptomatic leg, which was identical to the muscle carnitine response in normal subjects. In the patients' diseased leg, muscle short-chain acylcarnitine content increased with exercise from 440 +/- 130 to 900 +/- 200 (SE) nmol/g (P less than 0.05). In contrast to the nonsymptomatic leg, there was no increase in muscle lactate content in the diseased leg with exercise, and the change in muscle carnitine metabolism was correlated with exercise duration (r = 0.82, P less than 0.01) and not with the lactate threshold. We conclude that energy metabolism in ischemic muscle of patients with PAD is characterized by the accumulation of acylcarnitines.(ABSTRACT TRUNCATED AT 250 WORDS)

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Bartlett, Dr K., A. K. M. J. Bhuiyan, A. Aynsley-Green, P. C. Butler, and K. G. M. M. Alberti. "Human Forearm Arteriovenous Differences of Carnitine, Short-Chain Acylcarnitine and Long-Chain Acylcarnitine." Clinical Science 77, no. 4 (October 1, 1989): 413–16. http://dx.doi.org/10.1042/cs0770413.

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1. Forearm arterial and venous concentrations of free carnitine, short-chain acylcarnitine, long-chain acylcarnitine, glucose, lactate, pyruvate, alanine, non-esterified fatty acids, glycerol, 3-hydroxybutyrate and acetoacetate were measured in fasted adult subjects. 2. In all subjects there was net uptake of short-chain acylcarnitine, 3-hydroxybutyrate and acetoacetate and net release of free carnitine and non-esterified fatty acids. The arteriovenous differences of the other metabolites were not consistent. 3. These observations support the concept that short-chain acylcarnitine (largely acetylcarnitine) contributes to the flux of metabolic fuels from the liver to muscle in the fasted state, although to a limited extent in comparison with 3-hydroxybutyrate (< 5% on a molar basis).

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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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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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Brass, E. P., and S. P. Stabler. "Carnitine metabolism in the vitamin B-12-deficient rat." Biochemical Journal 255, no. 1 (October 1, 1988): 153–59. http://dx.doi.org/10.1042/bj2550153.

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In vitamin B-12 (cobalamin) deficiency the metabolism of propionyl-CoA and methylmalonyl-CoA are inhibited secondarily to decreased L-methylmalonyl-CoA mutase activity. Production of acylcarnitines provides a mechanism for removing acyl groups and liberating CoA under conditions of impaired acyl-CoA utilization. Carnitine metabolism was studied in the vitamin B-12-deficient rat to define the relationship between alterations in acylcarnitine generation and the development of methylmalonic aciduria. Urinary excretion of methylmalonic acid was increased 200-fold in vitamin B-12-deficient rats as compared with controls. Urinary acylcarnitine excretion was increased in the vitamin B-12-deficient animals by 70%. This increase in urinary acylcarnitine excretion correlated with the degree of metabolic impairment as measured by the urinary methylmalonic acid elimination. Urinary propionylcarnitine excretion averaged 11 nmol/day in control rats and 120 nmol/day in the vitamin B-12-deficient group. The fraction of total carnitine present as short-chain acylcarnitines in the plasma and liver of vitamin B-12-deficient rats was increased as compared with controls. When the rats were fasted for 48 h, relative or absolute increases were seen in the urine, plasma, liver and skeletal-muscle acylcarnitine content of the vitamin B-12-deficient rats as compared with controls. Thus vitamin B-12 deficiency was associated with a redistribution of carnitine towards acylcarnitines. Propionylcarnitine was a significant constituent of the acylcarnitine pool in the vitamin B-12-deficient animals. The changes in carnitine metabolism were consistent with the changes in CoA metabolism known to occur with vitamin B-12 deficiency. The vitamin B-12-deficient rat provides a model system for studying carnitine metabolism in the methylmalonic acidurias.

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Roe, D. S., N. Terada, and D. S. Millington. "Automated Analysis for Free and Short-Chain Acylcarnitine in Plasma with a Centrifugal Analyzer." Clinical Chemistry 38, no. 11 (November 1, 1992): 2215–20. http://dx.doi.org/10.1093/clinchem/38.11.2215.

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Abstract We describe a fully automated, spectrophotometric assay of free and total carnitine in plasma ultrafiltrates. The method, suitable for routine application in most hospital laboratories, incorporates the hydrolysis of acylcarnitines to free carnitine within the program of a Cobas Fara II centrifugal analyzer. The hydrolysis is monitored and calibrated with standard solutions containing octanoylcarnitine. Results correlated well with those from a reference isotope-dilution mass spectrometric assay. The ability to analyze a batch of samples for both free and total carnitine within 90 min enables analysis of > or = 100 samples per day. Used in conjunction with acylcarnitine species identification by mass spectrometry, the Cobas assay facilitates the diagnosis of carnitine-deficiency syndromes and specific metabolic disorders.

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Bhuiyan, A. K. M., K. Bartlett, H. S. A. Sherratt, and L. Agius. "Effects of ciprofibrate and 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA) on the distribution of carnitine and CoA and their acyl-esters and on enzyme activities in rats. Relation between hepatic carnitine concentration and carnitine acetyltransferase activity." Biochemical Journal 253, no. 2 (July 15, 1988): 337–43. http://dx.doi.org/10.1042/bj2530337.

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The effects of feeding the peroxisome proliferators ciprofibrate (a hypolipidaemic analogue of clofibrate) or POCA (2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate) (an inhibitor of CPT I) to rats for 5 days on the distribution of carnitine and acylcarnitine esters between liver, plasma and muscle and on hepatic CoA concentrations (free and acylated) and activities of carnitine acetyltransferase and acyl-CoA hydrolases were determined. Ciprofibrate and POCA increased hepatic [total CoA] by 2 and 2.5 times respectively, and [total carnitine] by 4.4 and 1.9 times respectively, but decreased plasma [carnitine] by 36-46%. POCA had no effect on either urinary excretion of acylcarnitine esters or [acylcarnitine] in skeletal muscle. By contrast, ciprofibrate decreased [acylcarnitine] and [total carnitine] in muscle. In liver, ciprofibrate increased the [carnitine]/[CoA] ratio and caused a larger increase in [acylcarnitine] (7-fold) than in [carnitine] (4-fold), thereby increasing the [short-chain acylcarnitine]/[carnitine] ratio. POCA did not affect the [carnitine]/[CoA] and the [short-chain acylcarnitine]/[carnitine] ratios, but it decreased the [long-chain acylcarnitine]/[carnitine] ratio. Ciprofibrate and POCA increased the activities of acyl-CoA hydrolases, and carnitine acetyltransferase activity was increased 28-fold and 6-fold by ciprofibrate and POCA respectively. In cultures of hepatocytes, ciprofibrate caused similar changes in enzyme activity to those observed in vivo, although [carnitine] decreased with time. The results suggest that: (1) the reactions catalysed by the short-chain carnitine acyltransferases, but not by the carnitine palmitoyltransferases, are near equilibrium in liver both before and after modification of metabolism by administration of ciprofibrate or POCA; (2) the increase in hepatic [carnitine] after ciprofibrate or POCA feeding can be explained by redistribution of carnitine between tissues; (3) the activity of carnitine acetyltransferase and [total carnitine] in liver are closely related.

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Bhattacharyya, Sudeepa, Mohamed Ali, William H. Smith, Paul E. Minkler, Maria S. Stoll, Charles L. Hoppel, and Sean H. Adams. "Anesthesia and bariatric surgery gut preparation alter plasma acylcarnitines reflective of mitochondrial fat and branched-chain amino acid oxidation." American Journal of Physiology-Endocrinology and Metabolism 313, no. 6 (December 1, 2017): E690—E698. http://dx.doi.org/10.1152/ajpendo.00222.2017.

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The period around bariatric surgery offers a unique opportunity to characterize metabolism responses to dynamic shifts in energy, gut function, and anesthesia. We analyzed plasma acylcarnitines in obese women ( n = 17) sampled in the overnight fasted/postabsorptive state approximately 1–2 wk before surgery ( condition A), the morning of surgery (prior restriction to a 48-h clear liquid diet coupled in some cases a standard polyethylene glycol gut evacuation: condition B), and following induction of anesthesia ( condition C). Comparisons tested if 1) plasma acylcarnitine derivatives reflective of fatty acid oxidation (FAO) and xenometabolism would be significantly increased and decreased, respectively, by preoperative gut preparation/negative energy balance ( condition A vs. B), and 2) anesthesia would acutely depress markers of FAO. Acylcarnitines associated with fat mobilization and FAO were significantly increased in condition B: long-chain acylcarnitines (i.e., C18:1, ~70%), metabolites from active but incomplete FAO [i.e., C14:1 (161%) and C14:2 (102%)] and medium- to short-chain acylcarnitines [i.e., C2 (91%), R-3-hydroxybutyryl-(245%), C6 (45%), and cis-3,4-methylene-heptanoyl-(17%), etc.]. Branched-chain amino acid markers displayed disparate patterns [i.e., isobutyryl-(40% decreased) vs. isovaleryl carnitine (51% increased)]. Anesthesia reduced virtually every acylcarnitine. These results are consistent with a fasting-type metabolic phenotype coincident with the presurgical “gut preparation” phase of bariatric surgery, and a major and rapid alteration of both fat and amino acid metabolism with onset of anesthesia. Whether presurgical or anesthesia-associated metabolic shifts in carnitine and fuel metabolism impact patient outcomes or surgical risks remains to be evaluated experimentally.

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Shigematsu, Yosuke, Miori Yuasa, Nobuyuki Ishige, Hideki Nakajima, and Go Tajima. "Development of Second-Tier Liquid Chromatography-Tandem Mass Spectrometry Analysis for Expanded Newborn Screening in Japan." International Journal of Neonatal Screening 7, no. 3 (July 14, 2021): 44. http://dx.doi.org/10.3390/ijns7030044.

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To minimize false-positive cases in newborn screening by tandem mass spectrometry in Japan, practical second-tier liquid chromatography-tandem mass spectrometry analyses have been developed using a multimode ODS column with a single set of mobile phases and different gradient elution programs specific to the analysis of acylcarnitines, acylglycines, amino acids, and organic acids. Most analyses were performed using underivatized samples, except for analysis of methylcitric acid, and careful conditioning of the column was necessary for analyses of organic acids. Our second-tier tests enabled us to measure many metabolites useful for detection of target disorders, including allo-isoleucine, homocysteine, methylmalonic acid, and methylcitric acid. We found that accumulation of 3-hydroxyglutaric acid was specific to glutaric acidemia type I and that the ratio of 3-hydroxyisovaleric acid to 3-hydroxyisovalerylcarnitine was useful to detect newborns of mothers with 3-methylcrotonyl-CoA carboxylase deficiency. Data from the analysis of short-chain acylcarnitine and acylglycine were useful for differential diagnosis in cases positive for C5-OH-acylcarnitine or C5-acylcarnitine.

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De Sousa, C., N. W. Y. Leung, R. A. Chalmers, and T. J. Peters. "Free and total carnitine and acylcarnitine content of plasma, urine, liver and muscle of alcoholics." Clinical Science 75, no. 4 (October 1, 1988): 437–40. http://dx.doi.org/10.1042/cs0750437.

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1. Plasma and urine free and total carnitine and acylcarnitine levels were assayed in 12 control subjects and 20 chronic alcoholics with fatty liver. Although the alcoholics had a wider range of values than the controls, there was no significant difference between the two groups. 2. Hepatic free and total carnitine and long- and short-chain acylcarnitines were assayed by a radioenzymatic method in samples from seven control subjects and seven alcoholics. No significant differences in any of the indices were noted between the patient and control groups and it was concluded that carnitine deficiency did not contribute to alcoholic fatty liver in patients without cirrhosis. 3. Skeletal muscle free and total carnitine and long-and short-chain acylcarnitines were assayed in eight alcoholics and seven control subjects. The alcoholics had significantly higher total and free carnitine levels. It is suggested that this reflects a selective enrichment of the biopsy sample with type I carnitine-rich fibres due to the type II fibre atrophy found in approximately half the patients.

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Afshinnia, Farsad, Thekkelnaycke M. Rajendiran, Tanu Soni, Jaeman Byun, Stefanie Wernisch, Kelli M. Sas, Jennifer Hawkins, et al. "Impaired β-Oxidation and Altered Complex Lipid Fatty Acid Partitioning with Advancing CKD." Journal of the American Society of Nephrology 29, no. 1 (October 11, 2017): 295–306. http://dx.doi.org/10.1681/asn.2017030350.

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Studies of lipids in CKD, including ESRD, have been limited to measures of conventional lipid profiles. We aimed to systematically identify 17 different lipid classes and associate the abundance thereof with alterations in acylcarnitines, a metric of β-oxidation, across stages of CKD. From the Clinical Phenotyping Resource and Biobank Core (CPROBE) cohort of 1235 adults, we selected a panel of 214 participants: 36 with stage 1 or 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 with stage 5 CKD. Among participants, 110 were men (51.4%), 64 were black (29.9%), and 150 were white (70.1%), and the mean (SD) age was 60 (16) years old. We measured plasma lipids and acylcarnitines using liquid chromatography-mass spectrometry. Overall, we identified 330 different lipids across 17 different classes. Compared with earlier stages, stage 5 CKD associated with a higher abundance of saturated C16–C20 free fatty acids (FFAs) and long polyunsaturated complex lipids. Long-chain–to–intermediate-chain acylcarnitine ratio, a marker of efficiency of β-oxidation, exhibited a graded decrease from stage 2 to 5 CKD (P<0.001). Additionally, multiple linear regression revealed that the long-chain–to–intermediate-chain acylcarnitine ratio inversely associated with polyunsaturated long complex lipid subclasses and the C16–C20 FFAs but directly associated with short complex lipids with fewer double bonds. We conclude that increased abundance of saturated C16–C20 FFAs coupled with impaired β-oxidation of FFAs and inverse partitioning into complex lipids may be mechanisms underpinning lipid metabolism changes that typify advancing CKD.

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Katrib, K., H. A. Adlouni, and G. Férard. "Presence of nonesterified and acylcarnitine in human polymorphonuclear leukocytes and mononuclear cells." Clinical Chemistry 33, no. 4 (April 1, 1987): 533–35. http://dx.doi.org/10.1093/clinchem/33.4.533.

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Abstract We demonstrate the presence of nonesterified carnitine and acylcarnitine in leukocytes, but not in erythrocytes, from 16 healthy adults. After carefully separating the different kinds of blood cells we measured significant amounts of nonesterified carnitine and acylcarnitine in polymorphonuclear leukocytes (28.5 +/- 6.1 and 18.5 +/- 6.3 mumol/10(9) cells) and mononuclear cells (25.4 +/- 5.2 and 14.8 +/- 4.5 mumol/10(9) cells). We also measured nonesterified carnitine, long-chain acylcarnitine, and short-chain acylcarnitine in plasma after fractionation with perchloric acid and obtained the following values (mean +/- SD): 41.4 +/- 2.6, 3.9 +/- 1.2, and 6.0 +/- 1.6 mumol/L, respectively. The mean percentages of total carnitine (n = 6) in polymorphonuclear leukocytes, mononuclear cells, and plasma were approximately 62%, 27%, and 13% of whole-blood carnitine, respectively (mean recovery was 102%). The percentage of acylated carnitine was 37% in leukocytes, as compared with 19% in plasma.

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Wolkowicz, P. E., D. F. Pauly, W. B. Van Winkle, and J. B. McMillin. "Chymotrypsin activates cardiac mitochondrial carnitine-acylcarnitine translocase." Biochemical Journal 261, no. 2 (July 15, 1989): 363–70. http://dx.doi.org/10.1042/bj2610363.

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The carnitine-acylcarnitine translocase facilitates carnitine and acylcarnitine transport into the mitochondrial matrix during beta-oxidation. Our results demonstrate that chymotrypsin can activate the maximal velocity of N-ethylmaleimide (NEM)-sensitive carnitine or palmitoylcarnitine exchange 7-fold, while doubling the affinity of the translocase for carnitine. Chymotrypsin activation is strictly dependent on the presence of free or short-chain acylcarnitine in the proteolysis medium, the extent of activation decreasing as the acylcarnitine chain length in the proteolysis medium increases. Chymotrypsin treatment decreases the apparent I50 value (inhibitor concentration required to give half-maximal inhibition) of the translocase for inhibition by NEM only under conditions which produce translocase activation. Modification of submitochondrial particle membranes by chymotrypsin does not result in gross ultrastructural changes or in an increase in the passive permeability of these membranes to carnitine. The data suggest that carnitine binding produces a change in translocase conformation which allows chymotrypsin modification to occur. This modification alters the kinetic and inhibitor-binding properties of the translocase.

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Adlouni, H. A., K. Katrib, and G. Férard. "Changes in carnitine in polymorphonuclear leukocytes, mononuclear cells, and plasma from patients with inflammatory disorders." Clinical Chemistry 34, no. 1 (January 1, 1988): 40–43. http://dx.doi.org/10.1093/clinchem/34.1.40.

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Abstract After finding relatively large amounts of carnitine in polymorphonuclear leukocytes and mononuclear cells from healthy subjects, we studied carnitine status in these cells and plasma from 20 patients with inflammatory disorders subsequent to multiple trauma and (or) head injury. The nonesterified carnitine content in polymorphonuclear leukocytes from patients significantly exceeded that in healthy subjects, while it was significantly decreased in mononuclear cells. In addition, the acylcarnitine content of both types of cells from patients was significantly increased. The total carnitine of polymorphonuclear leukocytes from patients was significantly increased, while that in mononuclear cells was unchanged, as compared with healthy subjects. In plasma from patients, nonesterified carnitine was extremely decreased, while both short-chain acylcarnitine and long-chain acylcarnitine were significantly increased. More than half of the carnitine was acylated in polymorphonuclear leukocytes and mononuclear cells in all patients tested, less than half in these cells from healthy subjects. Also, the presence of infection in these patients does increase, but not significantly, the nonesterified and acylcarnitine of both polymorphonuclear leukocytes and mononuclear cells from these patients.

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Tang, Minghua, Nicholas E. Weaver, Lillian M. Berman, Laura D. Brown, Audrey E. Hendricks, and Nancy F. Krebs. "Different Blood Metabolomics Profiles in Infants Consuming a Meat- or Dairy-Based Complementary Diet." Nutrients 13, no. 2 (January 27, 2021): 388. http://dx.doi.org/10.3390/nu13020388.

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Background: Research is limited in evaluating the mechanisms responsible for infant growth in response to different protein-rich foods; Methods: Targeted and untargeted metabolomics analysis were conducted on serum samples collected from an infant controlled-feeding trial that participants consumed a meat- vs. dairy-based complementary diet from 5 to 12 months of age, and followed up at 24 months. Results: Isoleucine, valine, phenylalanine increased and threonine decreased over time among all participants; Although none of the individual essential amino acids had a significant impact on changes in growth Z scores from 5 to 12 months, principal component heavily weighted by BCAAs (leucine, isoleucine, valine) and phenylalanine had a positive association with changes in length-for-age Z score from 5 to 12 months. Concentrations of acylcarnitine-C4, acylcarnitine-C5 and acylcarnitine-C5:1 significantly increased over time with the dietary intervention, but none of the acylcarnitines were associated with infant growth Z scores. Quantitative trimethylamine N-oxide increased in the meat group from 5 to 12 months; Conclusions: Our findings suggest that increasing total protein intake by providing protein-rich complementary foods was associated with increased concentrations of certain essential amino acids and short-chain acyl-carnitines. The sources of protein-rich foods (e.g., meat vs. dairy) did not appear to differentially impact serum metabolites, and comprehensive mechanistic investigations are needed to identify other contributors or mediators of the diet-induced infant growth trajectories.

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Park, Deung-Dae, Bernd M. Gahr, Julia Krause, Wolfgang Rottbauer, Tanja Zeller, and Steffen Just. "Long-Chain Acyl-Carnitines Interfere with Mitochondrial ATP Production Leading to Cardiac Dysfunction in Zebrafish." International Journal of Molecular Sciences 22, no. 16 (August 6, 2021): 8468. http://dx.doi.org/10.3390/ijms22168468.

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In the human heart, the energy supplied by the production of ATP is predominately accomplished by ß-oxidation in mitochondria, using fatty acids (FAs) as the primary fuel. Long-chain acylcarnitines (LCACs) are intermediate forms of FA transport that are essential for FA delivery from the cytosol into mitochondria. Here, we analyzed the impact of the LCACs C18 and C18:1 on mitochondrial function and, subsequently, on heart functionality in the in vivo vertebrate model system of zebrafish (Danio rerio). Since LCACs are formed and metabolized in mitochondria, we assessed mitochondrial morphology, structure and density in C18- and C18:1-treated zebrafish and found no mitochondrial alterations compared to control-treated (short-chain acylcarnitine, C3) zebrafish embryos. However, mitochondrial function and subsequently ATP production was severely impaired in C18- and C18:1-treated zebrafish embryos. Furthermore, we found that C18 and C18:1 treatment of zebrafish embryos led to significantly impaired cardiac contractile function, accompanied by reduced heart rate and diminished atrial and ventricular fractional shortening, without interfering with cardiomyocyte differentiation, specification and growth. In summary, our findings provide insights into the direct role of long-chain acylcarnitines on vertebrate heart function by interfering with regular mitochondrial function and thereby energy allocation in cardiomyocytes.

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Xu, Wei, Sandra Grindler, Sven Dänicke, Jana Frahm, Ákos Kenéz, and Korinna Huber. "Increased plasma and milk short-chain acylcarnitine concentrations reflect systemic LPS response in mid-lactation dairy cows." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 321, no. 3 (September 1, 2021): R429—R440. http://dx.doi.org/10.1152/ajpregu.00072.2021.

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Lipopolysaccharides (LPS) challenge the metabolic integrity of high-yielding dairy cows, activating the immune system and altering energy metabolism. Fatty acid oxidation, a major energy-gaining pathway, can be improved by supplementary carnitine, facilitating the transport of fatty acids into mitochondria. The metabolic response to the LPS challenge could alter both the plasma and the milk metabolome. Plasma and milk samples collected from cows treated with ( n = 27) or without ( n = 27) dietary carnitine, before and after intravenous administration of LPS, were subjected to a targeted metabolomics analysis. Multivariate statistical analyses revealed that both plasma and milk metabolome changed in response to the LPS challenge in both the carnitine-supplemented and the control cows. Short-chain acylcarnitines (carbon chain length C2, C3, C4, and C5) and long-chain acylcarnitines (C14, C16, and C18) had the highest performance to indicate LPS response when testing the predictive power of single metabolites using receiver-operator characteristics (ROC) analysis. The maximum area under a ROC curve (AUC) was 0.93. Biogenic amines, including sarcosine, and amino acids such as glutamine and isoleucine had AUC > 0.80 indicating metabolic changes due to the LPS challenge. In summary, the metabolites involved in the LPS response were acylcarnitines C2 and C5, sarcosine, glutamine, and isoleucine in plasma, and acylcarnitines C4 and C5 in milk. The interrelationship of plasma and milk metabolome included correlation of acylcarnitines C2, C4, and C5 between plasma and milk.

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Rossle, C., Y. A. Carpentier, M. Richelle, W. Dahlan, N. P. D'Attellis, P. Furst, and D. H. Elwyn. "Medium-chain triglycerides induce alterations in carnitine metabolism." American Journal of Physiology-Endocrinology and Metabolism 258, no. 6 (June 1, 1990): E944—E947. http://dx.doi.org/10.1152/ajpendo.1990.258.6.e944.

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Medium-chain triglycerides are generally assumed to be metabolized independently of carnitine. The effects of infusing medium-chain triglycerides on plasma concentrations of carnitine derivatives and beta-hydroxybutyrate were studied in four healthy male adults. Glucose and amino acids were infused alone for 3 h, then continued for another 5.5 h together with a lipid emulsion containing only long-chain triglycerides or a 50:50% (wt/wt) mixture of medium-chain and long-chain triglycerides. During the fat-free infusion, the concentration of free carnitine rose, whereas the level of acylcarnitines decreased. Infusion of the mixed emulsion over 5.5 h reduced free carnitine to lower values (32.4 +/- 4.7 mumols/l) than long-chain triglycerides infusion (44.4 +/- 2.7 mumol/l). By contrast, the plasma concentrations of short-chain acylcarnitine (12.1 +/- 3.3 vs. 5.4 +/- 1.9 mumols/l; P less than 0.01) and of beta-hydroxybutyrate (93 +/- 32 vs. 47 +/- 14 mumols/l; P less than 0.01) became significantly higher with the mixed emulsion than with long-chain triglycerides. This suggests that intravenous medium-chain triglycerides are not metabolized independently of carnitine. Carnitine may play an important role in removing acyl and acetyl groups from mitochondria and in restoring the intramitochondrial CoA level. Fat substrates are converted into compounds that might be utilized by tissues that do not normally oxidize fatty acids, creating an interorgan energy cycle.

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Lennon, D. L., and M. J. Mance. "Interorgan cooperativity in carnitine metabolism in the trained state." Journal of Applied Physiology 60, no. 5 (May 1, 1986): 1659–64. http://dx.doi.org/10.1152/jappl.1986.60.5.1659.

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This study was designed to evaluate the effects of chronic exercise training on carnitine acetyl- and palmitoyltransferase activity and the distribution of carnitine forms and concentrations in various organs and tissues of female rats. Sprague-Dawley rats were swim trained 6 days/wk and progressed to 75-min swims twice daily (with 3% of their total body weight attached to the medial portion of the tail) at the end of 5 wk of training. Sedentary (S, n = 12) and trained (T, n = 13) animals were killed by decapitation, and the livers, kidneys, hearts, and several skeletal muscle types were removed and immediately frozen in liquid N2 and/or extracted for enzyme activity assays. Blood was collected and plasma was stored frozen. Samples were assayed for free, acid-soluble, and acid-insoluble carnitine. Free carnitine increased significantly (P less than 0.03) in T hearts. Free carnitine remained unchanged in liver, but short-chain acylcarnitines increased significantly (P less than 0.001). There was a significant (P less than 0.001) reduction in long-chain acylcarnitines in kidney in the trained rats, and plasma short-chain acylcarnitine levels also decreased (P less than 0.001). Several significant changes in carnitine distribution also occurred in the superficial and deep portions of the vastus lateralis and in the mixed gastrocnemius muscles. There was a significant reduction in carnitine acetyltransferase activity with training in both the soleus (P less than 0.02) and superficial gastrocnemius (P less than 0.002) muscles. The deep portion of the gastrocnemius muscle contained significantly higher activity than either the superficial portion or the soleus.(ABSTRACT TRUNCATED AT 250 WORDS)

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Rousseau, Michèle, Frédéric Guénard, Véronique Garneau, Bénédicte Allam-Ndoul, Simone Lemieux, Louis Pérusse, and Marie-Claude Vohl. "Associations Between Dietary Protein Sources, Plasma BCAA and Short-Chain Acylcarnitine Levels in Adults." Nutrients 11, no. 1 (January 15, 2019): 173. http://dx.doi.org/10.3390/nu11010173.

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Elevated plasma branched-chain amino acids (BCAA) and C3 and C5 acylcarnitines (AC) levels observed in individuals with insulin resistance (IR) might be influenced by dietary protein intakes. This study explores the associations between dietary protein sources, plasma BCAA levels and C3 and C5 ACs in normal weight (NW) or overweight (OW) individuals with or without metabolic syndrome (MS). Data from 199 men and women aged 18–55 years with complete metabolite profile were analyzed. Associations between metabolic parameters, protein sources, plasma BCAA and AC levels were tested. OW/MS+ consumed significantly more animal protein (p = 0.0388) and had higher plasma BCAA levels (p < 0.0001) than OW/MS− or NW/MS− individuals. Plasma BCAA levels were not associated with BCAA intakes in the whole cohort, while there was a trend for an association between plasma BCAA levels and red meat or with animal protein in OW/MS+. These associations were of weak magnitude. In NW/MS− individuals, the protein sources associated with BCAA levels varied greatly with adjustment for confounders. Plasma C3 and C5 ACs were associated with plasma BCAA levels in the whole cohort (p < 0.0001) and in subgroups based on OW and MS status. These results suggest a modest association of meat or animal protein intakes and an association of C3 and C5 ACs with plasma BCAA levels, obesity and MS.

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Roe, Diane S., Charles R. Roe, Michèle Brivet, and Lawrence Sweetman. "Evidence for a Short-Chain Carnitine–Acylcarnitine Translocase in Mitochondria Specifically Related to the Metabolism of Branched-Chain Amino Acids." Molecular Genetics and Metabolism 69, no. 1 (January 2000): 69–75. http://dx.doi.org/10.1006/mgme.1999.2950.

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Ahmed, Ahmed T., Siamak Mahmoudian Dehkordi, Sudeepa Bhattacharyya, Matthias Arnold, Gregory Louie, Boadie Dunlop, Liewei Wang, et al. "T126. Short- Vs Medium + Long-Chain Plasma Acylcarnitine in Phenotypes of Major Depression at Baseline and After Citalopram/Escitalopram Treatment." Biological Psychiatry 85, no. 10 (May 2019): S177—S178. http://dx.doi.org/10.1016/j.biopsych.2019.03.449.

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Manta-Vogli, Penelope D., Kleopatra H. Schulpis, Yannis L. Loukas, and Yannis Dotsikas. "Perinatal free carnitine and short chain acylcarnitine blood concentrations in 12,000 full-term breastfed newborns in relation to their birth weight." Pediatrics & Neonatology 61, no. 6 (December 2020): 620–28. http://dx.doi.org/10.1016/j.pedneo.2020.07.015.

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Young, Sarah P., Dietrich Matern, Niels Gregersen, Robert D. Stevens, Deeksha Bali, Hui-Ming Liu, Dwight D. Koeberl, and David S. Millington. "A comparison of in vitro acylcarnitine profiling methods for the diagnosis of classical and variant short chain acyl-CoA dehydrogenase deficiency." Clinica Chimica Acta 337, no. 1-2 (November 2003): 103–13. http://dx.doi.org/10.1016/j.cccn.2003.07.006.

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Libert, Diane M., Amy S. Nowacki, and Marvin R. Natowicz. "Metabolomic analysis of obesity, metabolic syndrome, and type 2 diabetes: amino acid and acylcarnitine levels change along a spectrum of metabolic wellness." PeerJ 6 (August 31, 2018): e5410. http://dx.doi.org/10.7717/peerj.5410.

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Background Metabolic syndrome (MS) is a construct used to separate “healthy” from “unhealthy” obese patients, and is a major risk factor for type 2 diabetes (T2D) and cardiovascular disease. There is controversy over whether obese “metabolically well” persons have a higher morbidity and mortality than lean counterparts, suggesting that MS criteria do not completely describe physiologic risk factors or consequences of obesity. We hypothesized that metabolomic analysis of plasma would distinguish obese individuals with and without MS and T2D along a spectrum of obesity-associated metabolic derangements, supporting metabolomic analysis as a tool for a more detailed assessment of metabolic wellness than currently used MS criteria. Methods Fasting plasma samples from 90 adults were assigned to groups based on BMI and ATP III criteria for MS: (1) lean metabolically well (LMW; n = 24); (2) obese metabolically well (OBMW; n = 26); (3) obese metabolically unwell (OBMUW; n = 20); and (4) obese metabolically unwell with T2D (OBDM; n = 20). Forty-one amino acids/dipeptides, 33 acylcarnitines and 21 ratios were measured. Obesity and T2D effects were analyzed by Wilcoxon rank-sum tests comparing obese nondiabetics vs LMW, and OBDM vs nondiabetics, respectively. Metabolic unwellness was analyzed by Jonckheere-Terpstra trend tests, assuming worsening health from LMW → OBMW → OBMUW. To adjust for multiple comparisons, statistical significance was set at p < 0.005. K-means cluster analysis of aggregated amino acid and acylcarnitine data was also performed. Results Analytes and ratios significantly increasing in obesity, T2D, and with worsening health include: branched-chain amino acids (BCAAs), cystine, alpha-aminoadipic acid, phenylalanine, leucine + lysine, and short-chain acylcarnitines/total carnitines. Tyrosine, alanine and propionylcarnitine increase with obesity and metabolic unwellness. Asparagine and the tryptophan/large neutral amino acid ratio decrease with T2D and metabolic unwellness. Malonylcarnitine decreases in obesity and 3-OHbutyrylcarnitine increases in T2D; neither correlates with unwellness. Cluster analysis did not separate subjects into discreet groups based on metabolic wellness. Discussion Levels of 15 species and metabolite ratios trend significantly with worsening metabolic health; some are newly recognized. BCAAs, aromatic amino acids, lysine, and its metabolite, alpha-aminoadipate, increase with worsening health. The lysine pathway is distinct from BCAA metabolism, indicating that biochemical derangements associated with MS involve pathways besides those affected by BCAAs. Even those considered “obese, metabolically well” had metabolite levels which significantly trended towards those found in obese diabetics. Overall, this analysis yields a more granular view of metabolic wellness than the sole use of cardiometabolic MS parameters. This, in turn, suggests the possible utility of plasma metabolomic analysis for research and public health applications.

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Baraniuk, James N., Grant Kern, Vaishnavi Narayan, and Amrita Cheema. "Exercise modifies glutamate and other metabolic biomarkers in cerebrospinal fluid from Gulf War Illness and Myalgic encephalomyelitis / Chronic Fatigue Syndrome." PLOS ONE 16, no. 1 (January 13, 2021): e0244116. http://dx.doi.org/10.1371/journal.pone.0244116.

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Myalgic encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) share many symptoms of fatigue, pain, and cognitive dysfunction that are not relieved by rest. Patterns of serum metabolites in ME/CFS and GWI are different from control groups and suggest potential dysfunction of energy and lipid metabolism. The metabolomics of cerebrospinal fluid was contrasted between ME/CFS, GWI and sedentary controls in 2 sets of subjects who had lumbar punctures after either (a) rest or (b) submaximal exercise stress tests. Postexercise GWI and control subjects were subdivided according to acquired transient postexertional postural tachycardia. Banked cerebrospinal fluid specimens were assayed using Biocrates AbsoluteIDQ® p180 kits for quantitative targeted metabolomics studies of amino acids, amines, acylcarnitines, sphingolipids, lysophospholipids, alkyl and ether phosphocholines. Glutamate was significantly higher in the subgroup of postexercise GWI subjects who did not develop postural tachycardia after exercise compared to nonexercise and other postexercise groups. The only difference between nonexercise groups was higher lysoPC a C28:0 in GWI than ME/CFS suggesting this biochemical or phospholipase activities may have potential as a biomarker to distinguish between the 2 diseases. Exercise effects were suggested by elevation of short chain acylcarnitine C5-OH (C3-DC-M) in postexercise controls compared to nonexercise ME/CFS. Limitations include small subgroup sample sizes and absence of postexercise ME/CFS specimens. Mechanisms of glutamate neuroexcitotoxicity may contribute to neuropathology and “neuroinflammation” in the GWI subset who did not develop postural tachycardia after exercise. Dysfunctional lipid metabolism may distinguish the predominantly female ME/CFS group from predominantly male GWI subjects.

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Hiatt, W. R., J. G. Regensteiner, E. E. Wolfel, M. R. Carry, and E. P. Brass. "Effect of exercise training on skeletal muscle histology and metabolism in peripheral arterial disease." Journal of Applied Physiology 81, no. 2 (August 1, 1996): 780–88. http://dx.doi.org/10.1152/jappl.1996.81.2.780.

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Patients with symptomatic peripheral arterial occlusive disease have a claudication-limited peak exercise performance that is improved with exercise training. The effects of training on skeletal muscle metabolism were evaluated in 26 patients with claudication, randomized into a 12-wk program of treadmill training (enhances muscle metabolic activity in normal subjects), strength training (stimulates muscle hypertrophy in normal subjects), or a nonexercising control group. Gastrocnemius muscle biopsies were performed at rest and before and after training. After 12 wk, only treadmill training improved peak exercise performance and peak oxygen consumption. Treadmill training did not alter type I or type II fiber area and did not increase citrate synthase activity but was associated with an increase in the percentage of denervated fibers (from 7.6 +/- 5.4 to 15.6 +/- 7.5%, P < 0.05). Improvement in exercise performance with treadmill training was associated with a correlative decrease in the plasma (r = -0.67) and muscle (r = -0.59) short-chain acylcarnitine concentrations (intermediates of oxidative metabolism). Patients in the strength and control groups had no changes in muscle histology or carnitine metabolism, but strength-trained subjects had a decrease in citrate synthase activity. Thus treadmill training increased peak exercise performance, but this benefit was associated with skeletal muscle denervation and the absence of a "classic" mitochondrial training response (increase in citrate synthase activity). The present study confirms the relationship between skeletal muscle acylcarnitine content and function in peripheral arterial occlusive disease, demonstrating that the response to treadmill training was associated with parallel improvements in intermediary metabolism.

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Negrao, C. E., L. L. Ji, J. E. Schauer, F. J. Nagle, and H. A. Lardy. "Carnitine supplementation and depletion: tissue carnitines and enzymes in fatty acid oxidation." Journal of Applied Physiology 63, no. 1 (July 1, 1987): 315–21. http://dx.doi.org/10.1152/jappl.1987.63.1.315.

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Sixty-two male rats were randomly assigned into a 3 X 2 X 2 factorial design containing 12 groups according to carnitine treatment, exercise training (treadmill, 1 h, 5 times/wk, 8 wk, 26.8 m/min, 15% grade), and physical activity [rested for 60 h before they were killed or with an acute bout of exercise (1 h, 26.8 m/min, 15% grade) immediately before they were killed]. Isotonic saline was injected intraperitoneally 5 times/wk in the controls, whereas 750 mg/kg of L- or D-carnitine, respectively, were injected in the supplemented and depleted treatment groups. A significant increase in free and short-chain acyl carnitine concentration in skeletal muscle and heart was observed in L-carnitine supplemented rats, whereas a significant reduction in skeletal muscle, heart, and liver occurred in rats depleted of L-carnitine. Long-chain acyl carnitine in all tissues was not altered by carnitine treatment; training increased plasma and liver concentrations, whereas acute exercise decreased skeletal muscle and increased liver concentrations. An acute bout of exercise significantly increased short-chain acylcarnitine in liver, regardless of carnitine and/or training effects. beta-Hydroxyacyl-CoA dehydrogenase activity in skeletal muscle was induced by training but reduced by depletion. Carnitine acetyltransferase (CAT) was significantly increased in heart by L-carnitine supplementation, whereas it was reduced by depletion in skeletal muscle. Exercise training significantly increased CAT activity in skeletal muscle but not in heart, whereas acute exercise significantly increased activity in both tissues. Carnitine palmitoyltransferase activity was increased by acute exercise in the heart in only the supplemented and exercise-trained rats.

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Tosi, Irene, Tatiana Art, François Boemer, Dominique-Marie Votion, and Michael S. Davis. "Acylcarnitine profile in Alaskan sled dogs during submaximal multiday exercise points out metabolic flexibility and liver role in energy metabolism." PLOS ONE 16, no. 8 (August 12, 2021): e0256009. http://dx.doi.org/10.1371/journal.pone.0256009.

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Alaskan sled dogs develop a particular metabolic strategy during multiday submaximal exercise, allowing them to switch from intra-muscular to extra-muscular energy substrates thus postponing fatigue. Specifically, a progressively increasing stimulus for hepatic glycogenolysis and gluconeogenesis provides glucose for both fueling exercise and replenishing the depleted muscle glycogen. Moreover, recent studies have shown that with continuation of exercise sled dogs increase their insulin-sensitivity and their capacity to transport and oxidize glucose and carbohydrates rather than oxidizing fatty acids. Carnitine and acylcarnitines (AC) play an essential role as metabolic regulators in both fat and glucose metabolism; they serve as biomarkers in different species in both physiologic and pathologic conditions. We assessed the effect of multiday exercise in conditioned sled dogs on plasma short (SC), medium (MC) and long (LC) chain AC by tandem mass spectrometry (MS/MS). Our results show chain-specific modification of AC profiles during the exercise challenge: LCACs maintained a steady increase throughout exercise, some SCACs increased during the last phase of exercise and acetylcarnitine (C2) initially increased before decreasing during the later phase of exercise. We speculated that SCACs kinetics could reflect an increased protein catabolism and C2 pattern could reflect its hepatic uptake for energy-generating purposes to sustain gluconeogenesis. LCACs may be exported by muscle to avoid their accumulation to preserve glucose oxidation and insulin-sensitivity or they could be distributed by liver as energy substrates. These findings, although representing a “snapshot” of blood as a crossing point between different organs, shed further light on sled dogs metabolism that is liver-centric and more carbohydrate-dependent than fat-dependent and during prolonged submaximal exercise.

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Decombaz, J., B. Gmuender, G. Sierro, and P. Cerretelli. "Muscle carnitine after strenuous endurance exercise." Journal of Applied Physiology 72, no. 2 (February 1, 1992): 423–27. http://dx.doi.org/10.1152/jappl.1992.72.2.423.

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The effect of very long endurance exercise on muscle carnitine was studied. Eighteen cross-country skiers took part in a race in the Alps (average inspired partial pressure of O2 100–110 Torr) that lasted on average 13 h 26 min. Carnitine intake, evaluated for 2 wk before the event, was 50 +/- 4 (SE) mg/day. Muscle (vastus lateralis) total carnitine concentration, measured twice with a 2-yr interval on eight rested subjects, did not change with time (17 vs. 16 mumol/g dry wt, NS) but showed consistent interindividual differences (range 12–22, P = 0.001) with no correlation with intake. After exercise, total muscle carnitine was unaltered (from 17.9 +/- 1.0 at rest to 18.3 +/- 0.8 mumol/g dry wt postexercise in the 15 subjects who completed the race, NS), but muscle free carnitine decreased 20% (from 14.9 +/- 0.8 mumol/g, P = 0.01) and short-chain acylcarnitine increased 108% (from 3.5 +/- 0.4 mumol/g, P = 0.01). These results suggest that carnitine deficiency will probably not result from strenuous aerobic exercise in trained subjects who consume a moderate amount of carnitine in their food.

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Nagan, Narasimhan, Kent E. Kruckeberg, Angela L. Tauscher, Karen Snow Bailey, Piero Rinaldo, and Dietrich Matern. "The frequency of short-chain acyl-CoA dehydrogenase gene variants in the US population and correlation with the C4-acylcarnitine concentration in newborn blood spots." Molecular Genetics and Metabolism 78, no. 4 (April 2003): 239–46. http://dx.doi.org/10.1016/s1096-7192(03)00034-9.

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FERRER, I., P. RUIZSALA, Y. VICENTE, B. MERINERO, C. PEREZCERDA, and M. UGARTE. "Separation and identification of plasma short-chain acylcarnitine isomers by HPLC/MS/MS for the differential diagnosis of fatty acid oxidation defects and organic acidemias." Journal of Chromatography B 860, no. 1 (December 1, 2007): 121–26. http://dx.doi.org/10.1016/j.jchromb.2007.10.018.

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Zytkovicz, Thomas H., Eileen F. Fitzgerald, Deborah Marsden, Cecilia A. Larson, Vivian E. Shih, Donna M. Johnson, Arnold W. Strauss, Anne Marie Comeau, Roger B. Eaton, and George F. Grady. "Tandem Mass Spectrometric Analysis for Amino, Organic, and Fatty Acid Disorders in Newborn Dried Blood Spots." Clinical Chemistry 47, no. 11 (November 1, 2001): 1945–55. http://dx.doi.org/10.1093/clinchem/47.11.1945.

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Abstract Background: Tandem mass spectrometry (MS/MS) is rapidly being adopted by newborn screening programs to screen dried blood spots for >20 markers of disease in a single assay. Limited information is available for setting the marker cutoffs and for the resulting positive predictive values. Methods: We screened >160 000 newborns by MS/MS. The markers were extracted from blood spots into a methanol solution with deuterium-labeled internal standards and then were derivatized before analysis by MS/MS. Multiple reaction monitoring of each sample for the markers of interest was accomplished in ∼1.9 min. Cutoffs for each marker were set at 6–13 SD above the population mean. Results: We identified 22 babies with amino acid disorders (7 phenylketonuria, 11 hyperphenylalaninemia, 1 maple syrup urine disease, 1 hypermethioninemia, 1 arginosuccinate lyase deficiency, and 1 argininemia) and 20 infants with fatty and organic acid disorders (10 medium-chain acyl-CoA dehydrogenase deficiencies, 5 presumptive short-chain acyl-CoA dehydrogenase deficiencies, 2 propionic acidemias, 1 carnitine palmitoyltransferase II deficiency, 1 methylcrotonyl-CoA carboxylase deficiency, and 1 presumptive very-long chain acyl-CoA dehydrogenase deficiency). Approximately 0.3% of all newborns screened were flagged for either amino acid or acylcarnitine markers; approximately one-half of all the flagged infants were from the 5% of newborns who required neonatal intensive care or had birth weights <1500 g. Conclusions: In screening for 23 metabolic disorders by MS/MS, an mean positive predictive value of 8% can be achieved when using cutoffs for individual markers determined empirically on newborns.

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Wedekind, Roland, Agneta Kiss, Pekka Keski-Rahkonen, Vivian Viallon, Joseph A. Rothwell, Amanda J. Cross, Agnetha Linn Rostgaard-Hansen, et al. "A metabolomic study of red and processed meat intake and acylcarnitine concentrations in human urine and blood." American Journal of Clinical Nutrition 112, no. 2 (June 3, 2020): 381–88. http://dx.doi.org/10.1093/ajcn/nqaa140.

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ABSTRACT Background Acylcarnitines (ACs) play a major role in fatty acid metabolism and are potential markers of metabolic dysfunction with higher blood concentrations reported in obese and diabetic individuals. Diet, and in particular red and processed meat intake, has been shown to influence AC concentrations but data on the effect of meat consumption on AC concentrations is limited. Objectives To investigate the effect of red and processed meat intake on AC concentrations in plasma and urine using a randomized controlled trial with replication in an observational cohort. Methods In the randomized crossover trial, 12 volunteers successively consumed 2 different diets containing either pork or tofu for 3 d each. A panel of 44 ACs including several oxidized ACs was analyzed by LC-MS in plasma and urine samples collected after the 3-d period. ACs that were associated with pork intake were then measured in urine (n = 474) and serum samples (n = 451) from the European Prospective Investigation into Cancer and nutrition (EPIC) study and tested for associations with habitual red and processed meat intake derived from dietary questionnaires. Results In urine samples from the intervention study, pork intake was positively associated with concentrations of 18 short- and medium-chain ACs. Eleven of these were also positively associated with habitual red and processed meat intake in the EPIC cross-sectional study. In blood, C18:0 was positively associated with red meat intake in both the intervention study (q = 0.004, Student's t-test) and the cross-sectional study (q = 0.033, linear regression). Conclusions AC concentrations in urine and blood were associated with red meat intake in both a highly controlled intervention study and in subjects of a cross-sectional study. Our data on the role of meat intake on this important pathway of fatty acid and energy metabolism may help understanding the role of red meat consumption in the etiology of some chronic diseases. This trial was registered at Clinicaltrials.gov as NCT03354130.

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Soeters, Maarten R., Hans P. Sauerwein, Marinus Duran, Ronald J. Wanders, Mariëtte T. Ackermans, Eric Fliers, Sander M. Houten, and Mireille J. Serlie. "Muscle acylcarnitines during short-term fasting in lean healthy men." Clinical Science 116, no. 7 (March 2, 2009): 585–92. http://dx.doi.org/10.1042/cs20080433.

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The transition from the fed to the fasted resting state is characterized by, among other things, changes in lipid metabolism and peripheral insulin resistance. Acylcarnitines have been suggested to play a role in insulin resistance, as well as other long-chain fatty acid metabolites. Plasma levels of long-chain acylcarnitines increase during fasting, but this is unknown for muscle long-chain acylcarnitines. In the present study we investigated whether muscle long-chain acylcarnitines increase during fasting and we investigated their relationship with glucose/fat oxidation and insulin sensitivity in lean healthy humans. After 14 h and 62 h of fasting, glucose fluxes, substrate oxidation, and plasma and muscle acylcarnitines were measured before and during a hyperinsulinaemic–euglycaemic clamp. Hyperinsulinaemia decreased long-chain muscle acylcarnitines after 14 h of fasting, but not after 62 h of fasting. In both the basal state and during the clamp, glucose oxidation was lower and fatty acid oxidation was higher after 62 h compared with 14 h of fasting. Absolute changes in glucose and fatty acid oxidation in the basal compared with hyperinsulinaemic state were not different. Muscle long-chain acylcarnitines did not correlate with glucose oxidation, fatty acid oxidation or insulin-mediated peripheral glucose uptake. After 62 h of fasting, the suppression of muscle long-chain acylcarnitines by insulin was attenuated compared with 14 h of fasting. Muscle long-chain acylcarnitines do not unconditionally reflect fatty acid oxidation. The higher fatty acid oxidation during hyperinsulinaemia after 62 h compared with 14 h of fasting, although the absolute decrease in fatty acid oxidation was not different, suggests a different set point.

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Robinson, Lisa J., Janelle Zacherl, Harry C. Blair, and Stephanie J. Mihalik. "The Trans-Fatty Acid, Elaidic Acid, Inhibits Macrophage Fatty Acid Catabolism and Stimulates Expression of Inflammatory Mediators." Blood 120, no. 21 (November 16, 2012): 3277. http://dx.doi.org/10.1182/blood.v120.21.3277.3277.

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Abstract Abstract 3277 In recent decades, addition to the diet of synthetically hydrogenated vegetable oils has markedly increased human consumption of trans fatty acids. Epidemiological studies have linked this change in diet to current high rates of atherosclerotic cardiovascular disease. Despite recognition of this important connection, the basic mechanisms by which trans fatty acids contribute to the pathogenesis of atherosclerosis are still not well understood. In the present studies we examined the effects of trans fatty acids on macrophage functions and their possible role in the pathogenesis of atherosclerosis. Human macrophages, derived from peripheral blood mononuclear cells, were treated with the trans fat elaidic acid (C18:Δ9–10 trans), the corresponding cis fatty acid oleic acid (C18:Δ9–10 cis), or the saturated fatty acid stearic acid (C18:0). We examined changes in macrophage fat metabolism using GC/MS to measure cell fatty acid content and intermediates, and MS/MS to identify acylcarnitine derivatives, and assayed fatty acid oxidation using fatty acids radiolabeled at the [1–14C] position and the double bond at the [C9-C103H] position. After 44 hours treatment with 100 micromolar elaidic acid, macrophages showed an accumulation of multiple unsaturated fatty acid intermediates, both long-chain and short-chain, by GC/MS analysis, that were not observed in cultures containing either oleic or stearic acid. Using acylcarnitine analysis, we observed an increase in C12 and C18 intermediates in the macrophages exposed to trans fat (either as fatty acids or partially hydrogenated soy oil) compared to controls. These results suggest a block in acyl-CoA removal one group proximate to the trans bond. Beta-oxidation assays using carbon-1 radiolabeled oleic and elaidic acids revealed enhanced entry of the trans-fat into the catabolic cycle compared to the entry of the natural cis-fatty acid. Using carbon 9–10 radiolabeled oleic acid to study oleic acid catabolism, we discovered that in the presence of the trans fat, oxidation of the cis fat was diminished. Thus, in addition to the block in the catabolism of the trans fat itself, the degradation of the cis monounsaturated fatty acids are also impaired in the presence of the trans fat. We then examined the effects of inhibited fatty acid catabolism on macrophage function by examining changes in gene expression. Initial results from Affymetrix gene expression profiling, were confirmed using quantitative real time PCR. These studies revealed that exposure to trans fatty acid, compared to cis fatty acids, markedly upregulated macrophage expression of interleukin 1 beta, an inflammatory cytokine previously implicated in the pathogenesis of atherosclerosis. Also increased was expression of heparin-binding epidermal growth factor, previously implicated as a stimulus for vascular smooth muscle proliferation in atherosclerosis. The results overall suggest that the deleterious effects of trans fats may be linked to impaired macrophage fatty acid catabolism, contributing to lipid accumulation in the atheroma, and also to increased macrophage production of inflammatory mediators. Disclosures: No relevant conflicts of interest to declare.

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Cree-Green, Melanie, Anne-Marie Carreau, Haseeb Rahat, Yesenia Garcia-Reyes, Bryan C. Bergman, Laura Pyle, and Kristen J. Nadeau. "Amino acid and fatty acid metabolomic profile during fasting and hyperinsulinemia in girls with polycystic ovarian syndrome." American Journal of Physiology-Endocrinology and Metabolism 316, no. 5 (May 1, 2019): E707—E718. http://dx.doi.org/10.1152/ajpendo.00532.2018.

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Polycystic ovarian syndrome (PCOS) is associated with insulin resistance (IR) and altered muscle mitochondrial oxidative phosphorylation. IR in adults with obesity and diabetes is associated with changes in amino acid, free fatty acid (FFA), and mitochondrial acylcarnitine (AC) metabolism. We sought to determine whether these metabolites are associated with IR and/or androgens in youth-onset PCOS. We enrolled obese girls with PCOS [ n = 15, 14.5 yr (SD 1.6), %BMI 98.5 (SD 1.0)] and without PCOS [ n = 6, 13.2 yr (SD 1.2), %BMI 98.0 (SD 1.1)]. Insulin sensitivity was assessed by hyperinsulinemic euglycemic clamp. Untargeted metabolomics of plasma was performed while fasting and during hyperinsulinemia. Fasting arginine, glutamine, histidine, lysine, phenylalanine, and tyrosine were higher ( P < 0.04 for all but P < 0.001 for valine), as were glutamine and histidine during hyperinsulinemia ( P < 0.03). Higher valine during hyperinsulinemia was associated with IR ( r = 0.59, P = 0.006). Surprisingly, end-clamp AC C4 was lower in PCOS, and lower C4 was associated with IR ( r = −0.44, P = 0.04). End-clamp FFAs of C14:0, C16:1, and C18:1 were higher in PCOS girls, and C16:1 and C18:1 strongly associated with IR ( r = 0.73 and 0.53, P < 0.01). Free androgen index related negatively to short-, medium-, and long-chain AC ( r = −0.41 to −0.71, P < 0.01) but not FFA or amino acids. Obese girls with PCOS have a distinct metabolic signature during fasting and hyperinsulinemia. As in diabetes, IR related to valine and FFAs, with an unexpected relationship with AC C4, suggesting unique metabolism in obese girls with PCOS.

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Palladino, Andrew A., Michael J. Bennett, and Charles A. Stanley. "Hyperinsulinism in Infancy and Childhood: When an Insulin Level Is Not Always Enough." Clinical Chemistry 54, no. 2 (February 1, 2008): 256–63. http://dx.doi.org/10.1373/clinchem.2007.098988.

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Abstract Background: Hypoglycemia in infants and children can lead to seizures, developmental delay, and permanent brain damage. Hyperinsulinism (HI) is the most common cause of both transient and permanent disorders of hypoglycemia. HI is characterized by dysregulated insulin secretion, which results in persistent mild to severe hypoglycemia. The various forms of HI represent a group of clinically, genetically, and morphologically heterogeneous disorders. Content: Congenital hyperinsulinism is associated with mutations of SUR-1 and Kir6.2, glucokinase, glutamate dehydrogenase, short-chain 3-hydroxyacyl-CoA dehydrogenase, and ectopic expression on β-cell plasma membrane of SLC16A1. Hyperinsulinism can be associated with perinatal stress such as birth asphyxia, maternal toxemia, prematurity, or intrauterine growth retardation, resulting in prolonged neonatal hypoglycemia. Mimickers of hyperinsulinism include neonatal panhypopituitarism, drug-induced hypoglycemia, insulinoma, antiinsulin and insulin-receptor stimulating antibodies, Beckwith-Wiedemann Syndrome, and congenital disorders of glycosylation. Laboratory testing for hyperinsulinism may include quantification of blood glucose, plasma insulin, plasma β-hydroxybutyrate, plasma fatty acids, plasma ammonia, plasma acylcarnitine profile, and urine organic acids. Genetic testing is available through commercial laboratories for genes known to be associated with hyperinsulinism. Acute insulin response (AIR) tests are useful in phenotypic characterization. Imaging and histologic tools are also available for diagnosing and classifying hyperinsulinism. The goal of treatment in infants with hyperinsulinism is to prevent brain damage from hypoglycemia by maintaining plasma glucose levels above 700 mg/L (70 mg/dL) through pharmacologic or surgical therapy. Summary: The management of hyperinsulinism requires a multidisciplinary approach that includes pediatric endocrinologists, radiologists, surgeons, and pathologists who are trained in diagnosing, identifying, and treating hyperinsulinism.

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Valkner, K., S. Ely, J. Kerner, J. Scott, and L. L. Bieber. "Effect of hypoxia on pig heart short-chain acylcarnitines." Comparative Biochemistry and Physiology Part A: Physiology 80, no. 1 (January 1985): 123–27. http://dx.doi.org/10.1016/0300-9629(85)90689-9.

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Diab, J., T. Hansen, R. Goll, H. Stenlund, E. Jensen, T. Moritz, J. Florholmen, and G. Forsdahl. "P003 Metabolomics for improved patient stratification in inflammatory bowel disease: Characterisation of the ulcerative colitis metabolome." Journal of Crohn's and Colitis 14, Supplement_1 (January 2020): S130—S131. http://dx.doi.org/10.1093/ecco-jcc/jjz203.132.

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Abstract Background The onset of ulcerative colitis (UC) is characterised by a dysregulated mucosal immune response triggered by several genetic and environmental factors in the context of host-microbe interaction. This complexity makes UC ideal for metabolomic studies to unravel the disease pathobiology and to improve the patient stratification strategies toward personalised medicine. This study aims to explore the mucosal metabolomic profile in treatment-naïve and deep remission UC patients, and to define the metabolic signature of UC. Methods Treatment-naive UC patients (n = 18), UC patients in deep remission (n = 10), and healthy volunteers (n = 14) were recruited. Mucosa biopsies were collected during colonoscopy. The UC activity and the state of deep remission were assessed by endoscopy, histology, and by measuring TNF gene expression. Metabolomic analysis was performed by combined gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF-MS) and ultra-high performance liquid chromatography coupled with mass spectrometry (UHPLC-MS). In total, 177 metabolites from 50 metabolic pathways were identified. Results Multivariate data analysis revealed a distinct metabolomic profile in inflamed mucosa taken from treatment- naïve UC patients compared with non-inflamed mucosa taken from UC remission patients and healthy controls. The mucosal metabolome in UC remission patients differed to a lesser extent from the healthy controls. The most prominent metabolome changes among the study groups were in lysophosphatidylcholine, acylcarnitine, and amino acid profiles. Several metabolic pathways were perturbed, ranging from amino acid metabolism (such as tryptophan metabolism, and alanine, aspartate and glutamate metabolism) to antioxidant defence pathway (glutathione pathway). Furthermore, the pathway analysis revealed a disruption in the long-and short-chain fatty acid (LCFA and SCFA) metabolism, namely linoleic metabolism and butyrate metabolism. Conclusion The mucosal metabolomic profiling revealed a metabolic signature during the onset of UC, and reflected the homeostatic disturbance in the gut. The altered metabolic pathways highlight the importance of system biology approaches to identify key drivers of IBD pathogenesis which prerequisite personalised treatment.

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Servillo, Luigi, Nunzia D’Onofrio, Gianluca Neglia, Rosario Casale, Domenico Cautela, Massimo Marrelli, Antonio Limone, Giuseppe Campanile, and Maria Luisa Balestrieri. "Carnitine Precursors and Short-Chain Acylcarnitines in Water Buffalo Milk." Journal of Agricultural and Food Chemistry 66, no. 30 (July 16, 2018): 8142–49. http://dx.doi.org/10.1021/acs.jafc.8b02963.

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Waagsbø, Bjørn, Asbjørn Svardal, Thor Ueland, Linn Landrø, Olav Øktedalen, Rolf K. Berge, Trude H. Flo, Pål Aukrust, and Jan K. Damås. "Low levels of short- and medium-chain acylcarnitines in HIV-infected patients." European Journal of Clinical Investigation 46, no. 5 (March 7, 2016): 408–17. http://dx.doi.org/10.1111/eci.12609.

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Owei, Ibiye, Nkiru Umekwe, Frankie Stentz, Jim Wan, and Sam Dagogo-Jack. "Association of plasma acylcarnitines with insulin sensitivity, insulin secretion, and prediabetes in a biracial cohort." Experimental Biology and Medicine 246, no. 15 (April 29, 2021): 1698–705. http://dx.doi.org/10.1177/15353702211009493.

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The ability to predict prediabetes, which affects ∼90 million adults in the US and ∼400 million adults worldwide, would be valuable to public health. Acylcarnitines, fatty acid metabolites, have been associated with type 2 diabetes risk in cross-sectional studies of mostly Caucasian subjects, but prospective studies on their link to prediabetes in diverse populations are lacking. Here, we determined the association of plasma acylcarnitines with incident prediabetes in African Americans and European Americans enrolled in a prospective study. We analyzed 45 acylcarnitines in baseline plasma samples from 70 adults (35 African-American, 35 European-American) with incident prediabetes (progressors) and 70 matched controls (non-progressors) during 5.5-year (mean 2.6 years) follow-up in the Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) study. Incident prediabetes (impaired fasting glucose/impaired glucose tolerance) was confirmed with OGTT. We measured acylcarnitines using tandem mass spectrometry, insulin sensitivity by hyperinsulinemic euglycemic clamp, and insulin secretion using intravenous glucose tolerance test. The results showed that progressors and non-progressors during POP-ABC study follow-up were concordant for 36 acylcarnitines and discordant for nine others. In logistic regression models, beta-hydroxy butyryl carnitine (C4-OH), 3-hydroxy-isovaleryl carnitine/malonyl carnitine (C5-OH/C3-DC), and octenoyl carnitine (C8:1) were the only significant predictors of incident prediabetes. The combined cut-off plasma levels of <0.03 micromol/L for C4-OH, <0.03 micromol/L for C5-OH/C3-DC, and >0.25 micromol/L for C8:1 acylcarnitines predicted incident prediabetes with 81.9% sensitivity and 65.2% specificity. Thus, circulating levels of one medium-chain and two short-chain acylcarnitines may be sensitive biomarkers for the risk of incident prediabetes among initially normoglycemic individuals with parental history of type 2 diabetes.

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Meadows, Jamie A., Graham G. Willsey, and Matthew J. Wargo. "Differential requirements for processing and transport of short-chain versus long-chain O-acylcarnitines in Pseudomonas aeruginosa." Microbiology 164, no. 4 (April 1, 2018): 635–45. http://dx.doi.org/10.1099/mic.0.000638.

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RAZO-AZAMAR, MELISSA, RAFAEL NAMBO-VENEGAS, JAIME DELGADILLO-VELAZQUEZ, and BERENICE PALACIOS-GONZALEZ. "2422-PUB: Short-Chain Acylcarnitines as Early Predictors of Gestational Diabetes in Mexican Population." Diabetes 68, Supplement 1 (June 2019): 2422—PUB. http://dx.doi.org/10.2337/db19-2422-pub.

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Langenau, Boeing, Bergmann, Nöthlings, and Oluwagbemigun. "The Association between Alcohol Consumption and Serum Metabolites and the Modifying Effect of Smoking." Nutrients 11, no. 10 (October 1, 2019): 2331. http://dx.doi.org/10.3390/nu11102331.

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Alcohol consumption is an important lifestyle factor that is associated with several health conditions and a behavioral link with smoking is well established. Metabolic alterations after alcohol consumption have yet to be comprehensively investigated. We studied the association of alcohol consumption with metabolite patterns (MPs) among 2433 individuals from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study, and a potential modification by smoking. Alcohol consumption was self-reported through dietary questionnaires and serum metabolites were measured by a targeted approach. The metabolites were summarized as MPs using the treelet transform analysis (TT). We fitted linear models with alcohol consumption continuously and in five categories. We stratified the continuously modelled alcohol consumption by smoking status. All models were adjusted for potential confounders. Among men, alcohol consumption was positively associated with six MPs and negatively associated with one MP. In women, alcohol consumption was inversely associated with one MP. Heavy consumers differed from other consumers with respect to the “Long and short chain acylcarnitines” MP. Our findings suggest that long and short chain acylcarnitines might play an important role in the adverse effects of heavy alcohol consumption on chronic diseases. The relations seem to depend on gender and smoking status.

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Sauer, Sven Wolfgang, Juergen G. Okun, Georg F. Hoffmann, Stefan Koelker, and Marina A. Morath. "Impact of short- and medium-chain organic acids, acylcarnitines, and acyl-CoAs onmitochondrial energy metabolism." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1777, no. 10 (October 2008): 1276–82. http://dx.doi.org/10.1016/j.bbabio.2008.05.447.

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Teren, Andrej, Anika Vogel, Frank Beutner, Stephan Gielen, Ralph Burkhardt, Markus Scholz, Joachim Thiery, and Uta Ceglarek. "Relationship between fermented dairy consumption, circulating short-chain acylcarnitines and angiographic severity of coronary artery disease." Nutrition, Metabolism and Cardiovascular Diseases 30, no. 10 (September 2020): 1662–72. http://dx.doi.org/10.1016/j.numecd.2020.05.031.

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Journal articles on the topic 'Short chain acylcarnitine'

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