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Acetylcarnitine and free carnitine in body fluids before and after birth.

The acetylcarnitine concentration in amniotic fluid fell significantly between 33 and 37 and 40 weeks of gestation. It was significantly higher in samples that had a low lecithin to sphingomyelin ratio. The acetylcarnitine content of tracheal fluid was higher in samples obtained from premature newborns. The major excretory form of carnitine is the acetate ester and only in adults does the urine contain significant amounts of free carnitine. The level of acetylcarnitine in plasma significantly increases after the first day of life; there was no difference in the plasma levels of carnitine between full-term and premature newborns. Plasma-free carnitine and acetylcarnitine levels were significantly lower in infants who were receiving a soybean-based formula. A positive correlation was found between the plasma level of ketone bodies and that of acetylcarnitine.

Acetylcarnitine

Enzymic hydrolysis of acetylcarnitine in liver from rats, sheep and cows.

1. The enzymic utilization of O-acetyl-l-carnitine other than via carnitine acetyltransferase (EC 2.3.1.7) was investigated in liver homogenates from rats, sheep and dry cows. 2. An enzymic utilization of O-acetyl-l-carnitine via hydrolysis of the ester bond to yield stoicheiometric quantities of acetate and l-carnitine was demonstrated; 0.55, 0.53 and 0.30mumol of acetyl-l-carnitine were utilized/min per g fresh wt. of liver homogenates from rats, sheep and dry cows respectively. 3. The acetylcarnitine hydrolysis activity was not due to a non-specific esterase or non-specific cholinesterase. O-Acetyl-d-carnitine was not utilized. 4. The activity was associated with the enriched outer mitochondrial membrane fraction from rat liver. Isolation of this fraction resulted in an eightfold purification of acetylcarnitine hydrolase activity. 4. The K(m) for this acetylcarnitine utilization was 2mm and 1.5mm for rat and sheep liver homogenates respectively. 6. There was a significant increase in acetylcarnitine hydrolase in rats on starvation and cows on lactation and a significant decrease in sheep that were severely alloxan-diabetic. 7. The physiological role of an acetylcarnitine hydrolase is discussed in relation to coupling with carnitine acetyltransferase for the relief of ;acetyl pressure'.

Animals

The concentrations of free L-carnitine and L-O-acetylcarnitine in spermatozoa and seminal plasma of normal, fresh, and frozen human semen.

Free-L-carnitine and L-O-acetylcarnitine concentrations have been determined in spermatozoa and seminal plasma of normal, fresh, and frozen human semen. Results show that in fresh semen most of the free L-carnitine (0.213 +/- 0.02 mM) and L-O-acetylcarnitine (0.063 +/- 0.007 mM) is found in the seminal plasma. In contrast to other worker's results, the concentrations of free L-carnitine and L-O-acetylcarnitine in spermatozoa were found to be high and were 0.384 +/- 0.066 mumole/10(9) spermatozoa (22 mM) and 0.376 +/- 0.057 mumole/10(9) spermatozoa (21.6 mM), respectively. It is also demonstrated that the distribution of soluble metabolites such as L-carnitine between spermatozoa and seminal plasma is altered by the freezing of semen. After freezing and storage of semen at -20 degrees C for 7 days, the intracellular concentrations of free L-carnitine and L-O-acetylcarnitine decreased to below the limits of assay.

Acetylcarnitine

Deacylation of acetyl-coenzyme A and acetylcarnitine by liver preparations.

The breakdown of acetylcarnitine catalysed by extracts of rat and sheep liver was completely abolished by Sephadex G-25 gel filtration, whereas the hydrolysis of acetyl-CoA was unaffected. Acetyl-CoA and CoA acted catalytically in restoring the ability of Sephadex-treated extracts to break down acetylcarnitine, which was therefore not due to an acetylcarnitine hydrolase but to the sequential action of carnitine acetyltransferase and acetyl-CoA hydrolase. Some 75% of the acetyl-CoA hydrolase activity of sheep liver was localized in the mitochondrial fraction. Two distinct acetyl-CoA hydrolases were partially purified from extracts of sheep liver mitochondria. Both enzymes hydrolysed other short-chain acyl-CoA compounds and succinyl-CoA (3-carboxypropionyl-CoA), but with one acetyl-CoA was the preferred substrate.

Acetates

Carnitine, acetylcarnitine and the activity of carnitine acyltransferases in seminal plasma and spermatozoa of men, rams and rats.

The concentration of total carnitine (i.e. carnitine plus acetylcarnitine) was measured in seminal plasma and spermatozoa of men and rams. In ram semen, there was a close correlation between the concentration of spermatozoa and that of total carnitine in the seminal plasma, indicating that the epididymal secretion was the sole source of seminal carnitine. The percentage of total carnitine present as acetylcarnitine was 40% in seminal plasma and 70-80% in spermatozoa. The acetylation state of carnitine in seminal plasma was apparently not influenced by the metabolic activity of spermatozoa in ejaculated ram semen as no change was found in the plasma concentration of carnitine or acetylcarnitine up to 45 min after ejaculation. In spermatozoa, the activity of carnitine acetyltransferase (EC 2.3.1.7) was approximately equivalent to that of carnitine palmitoyltransferase (EC 2.3.1.21); and the activity of these enzymes was similar in ram and human spermatozoa but greater in rat spermatozoa. It is concluded that there is no correlation between the content of either total carnitine or the carnitine acyltransferases and the respiratory capacity of spermatozoa.

Acetylcarnitine

Levels of L-carnitine and L-O-acetylcarnitine in normal and infertile human semen: a lower level of L-O-acetycarnitine in infertile semen.

The level of total L-carnitine was determined in normal human seminal plasma and sperm. Most of the L-carnitine is concentrated in the seminal plasma and its level is about 10 times higher than that in blood plasma. About 50% of total L-carnitine in normal human seminal plasma exists in the form of acetylcarnitine. Similar studies were also carried out in oligospermic and azoospermic human seminal plasma. The level of L-O-acetylcarnitine in both types of infertile samples is significantly lower than that in normal samples. On the other hand, the level of free L-carnitine is the same in fertile and infertile seminal plasma.

Acetylcarnitine

The distribution of carnitine and acetylcarnitine in the rabbit epididymis and the carnitine content of rabbit spermatozoa during maturation.

The highest levels of carnitine and acetylcarnitine were found in the cauda, and spermatozoa from the proximal cauda contained significantly greater amounts of carnitine than those removed from the corpus or caput epididymidis. Acetylcarnitine levels (as a % of the total carnitine pool) were greater in all regions of the rabbit epididymis than has been reported in other species. It is suggested that the accumulation of carnitine is involved in sperm maturation.

Acetylcarnitine

Carnitine and acetylcarnitine in skeletal and cardiac muscle.

The acetylcarnitine/carnitine ratio has been found significantly increased in tibial muscles of swimming rats in comparison with normal rats. Analogous increase occurred in electrically stimulated tibial muscle in comparison with the unstimulated controlateral muscle of the same animal. Swimming also induced a statistically significant increase of the acetylcarnitine/carnitine ratio in heart, while norepinephrine administration resulted in a decrease of carnitine not accompanied by a corresponding increase in acetylcarnitine in a severe carnitine depletion of cardiac muscle. These results are discussed in terms of carnitine function in the acetyl metabolism, assuming the acetylcarnitine as a possible acetyl reservoir in the working muscle.

Acetylcarnitine

In vitro stimulation of human sperm motility by acetylcarnitine.

An increase in motility of ejaculated human spermatozoa was observed after the addition of acetylcaritine or carnitine. Similar results were also obtained in the diluted semen with 25--30% initial motilities. However, indirect evidence suggests that carnitine is converted to acetylcarnitine prior to its stimulatory action. In addition, this stimulation was shown to be the result of no increase in ionic strength nor any change in the levels of ATP.

Acetylcarnitine

Mitochondrial metabolism of pyruvate in bovine spermatozoa.

Treatment with the polyene antibiotic, filipin, renders the spermatozoan cell membrane permeable to small molecules, but not to the intracellular enzymes aldolase and lactate dehydrogenase. Pyruvate (10 mM) as the sole substrate was metabolized very slowly. L-Carnitine increased pyruvate metabolism 3- to 4-fold and allowed limited rates of oxidative phosphorylation. When spermatozoa treated with filipin were supplemented with malate, there was a rapid, almost linear rate of pyruvate metabolism which was slightly increased by L-carnitine. In the absence of malate, 20 to 30% of the pyruvate used was reduced to lactate; this increased to 57% in the presence of malate. Without malate, about 90% of the pyruvate metabolized was converted to lactate and acetate or L-acetylcarnitine. Rutamycin or rotenone increased both the rate of pyruvate use and the delta lactate/deltapyruvate ratio. Under all treatments, L-carnitine consistently reduced the percentage of pyruvate converted to lactate by about 10%; part of the pyruvate was preferentially shunted into L-acetylcarnitine rather than lactate. The mitochondrial inhibitors, rotenone or rutamycin, did not change the amount of pyruvate that was converted to metabolites other than lactate, or L-acetylcarnitine, or both. Pyruvate-supported State 3 respiration was linear only if L-carnitine, or malate, or both, were added to the incubation medium. Added malate was necessary to produce a rapid State 3 respiratory rate and was also required for significant respiratory activity in the presence of rotenone or rutamycin. From cells metabolizing [2-14C]pyruvate (1.4 mM), 14C-labeled acid-extractable metabolites were separated by ion exchange column chromatography. All of the [2-14C]pyruvate (+/-5%) used was recovered in 14C-labeled metabolites and 14CO2. In the presence of malate, citrate accumulation was significant, and was always large in comparison to flux through the citric acid cycle. Glutamate, beta-hydroxybutyrate, acetoacetate, fumarate, aspartate, and alpha-ketoglutarate did not accumulate in significant amounts. Some 14C-labeled succinate was produced but only in the presence of malate. Alkaline hydrolysis of a fraction containing carnitine esters yielded acetate and a compound tentatively identified as beta-hydroxybutyrate or lactate. As in intact cells, intramitochondrial lactate dehydrogenase competes successfully with the electron transport system for the NADH generated by pyruvate metabolism. The role of lactate and L-carnitine, and conclusions suggested by the accumulation of certain metabolites are discussed in relation to control of citric acid cycle activity.

Acetates

Hypothesis-free evaluation of circulating metabolome provides cell-specific insights regarding the role of energy substrate availability in amyotrophic lateral sclerosis.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with limited therapeutic options. The circulating metabolome comprises small molecules present in plasma/serum which are the intermediates and end-products of cellular metabolism, and is linked to ALS pathogenesis. METHODS: We conducted hypothesis-free two-sample Mendelian randomisation (MR) analysis of the concentration of 575 plasma/serum metabolites, to determine which are causally linked to risk of ALS. Significant metabolites were validated in an independent GWAS of plasma/serum metabolite concentrations and evaluated for sex-specific effects. Correlations between directly measured patient biofluid metabolite concentrations and ALS risk/severity were examined in 94 ALS patients and 40 controls. We experimentally assessed metabolic function in a murine neurons and human astrocytes carrying an ALS-associated G4C2-repeat expansion within C9orf72. RESULTS: MR causally associated five metabolites with ALS risk after multiple-testing correction. Higher serum concentration of glycoprotein acetyls (P&#x2009;=&#x2009;9.7e&#x2009;-&#x2009;9, &#x3b2;&#x2009;=&#x2009;0.21) and the peptide DSGEGDFXAEGGGVR (P&#x2009;=&#x2009;8.0e&#x2009;-&#x2009;6, &#x3b2;&#x2009;=&#x2009;0.22) was associated with increased ALS risk, whereas higher plasma concentration of phenylalanylserine, isobutyrylcarnitine, and acetylcarnitine was protective (P&#x2009;<&#x2009;5e&#x2009;-&#x2009;5, &#x3b2;&#x2009;= -&#x2009;0.29 to&#x2009;-&#x2009;0.72). DSGEGDFXAEGGGVR has been linked to glucose metabolism but we have used genetic fine-mapping to link DSGEGDFXAEGGGVR, neuronal glucose uptake through GLUT3, and ALS risk. Direct measurement of metabolite concentrations in patient biofluids revealed elevated acetylcarnitine levels in patients with ALS, which were associated with delayed symptom onset (Cox regression, P&#x2009;=&#x2009;0.02, HR&#x2009;=&#x2009;0.4). Similarly, lactate is elevated in ALS patient CSF (ANOVA, P&#x2009;=&#x2009;1.3e&#x2009;-&#x2009;3) and in patients with longer survival time (Cox regression, P&#x2009;=&#x2009;0.03, HR&#x2009;=&#x2009;0.3). Plasma fructose is elevated in ALS patients with shorter survival time (Cox regression, P&#x2009;=&#x2009;0.02, HR&#x2009;=&#x2009;1.1). In vitro, neurons and astrocytes carrying an ALS-associated G4C2-repeat expansion within C9orf72 demonstrated reduced metabolic flexibility. CONCLUSIONS: We provide evidence that impaired energy substrate availability contributes to ALS risk and severity. CNS cell types differ in their use of energy substrates and therefore we postulate the relative importance of different cell types for different stages of disease. Our findings support further investigation of metabolic interventions to treat or prevent ALS.

Amyotrophic Lateral Sclerosis

Effect of clofibrate treatment on acylcarnitine oxidation in isolated rat liver mitochondria.

The oxidation of palmitoyl- and octanoylcarnitine in liver mitochondria from normal and clofibrate-treated male rats was studied by measuring the ADP-stimulated oxygen consumption and acetyl group production (the sum of formed ketone bodies, acetylcarnitine and citrate). In the absence of malate the treatment approximately doubled the rate of acylcarnitine oxidation. In normal mitochondria the acetyl groups consisted almost totally of ketone bodies. The clofibrate-induced increase in acetyl group production was attributable to enhanced rates of ketone body and acetylcarnitine formation. The observed increase in acylcarnitine oxidation was associated with an elevated beta-hydroxybutyrate: acetoacetate ratio, reflecting an increased mitochondrial NADH:NAD+ ratio. In normal mitochondria the addition of malate in the presence of fluorocitrate doubled the rate of beta oxidation by forming citrate. The beta oxidation in mitochondria from clofibrate-treated rats was virtually unresponsive to added malate. The clofibrate-induced increase in ketogenesis was confirmed in disintegrated mitochondria. The treatment approximately doubled the rate of ketone body production from acetyl-CoA in disrupted organelles. The enhanced capacity of ketogenesis was accompanied by increased activity of the specific acetoacetyl-CoA thiolase (EC 2.3.1.8), which is the first step enzyme of the pathway. Clofibrate administration also increased the activities of general oxoacyl-CoA thiolase (EC 2.3.1.16), palmitoyl-CoA dehydrogenase (EC 1.3.99.3), and butyryl-CoA dehydrogenase (EC 1.3.99.2), which all take part in the beta oxidation of fatty acids.

Acetoacetates

Pulmonary fatty acid synthesis. I. Mitochondrial acetyl transfer by rat lung in vitro.

Incorporation of tritiated water into fatty acids by rat adipose tissue and lung tissue slices incubated with 5 mM glucose indicated a level of fatty acid synthesis in rat lung approximately 15% that observed in adipose tissue in vitro. (-)-Hydroxycitrate, and inhibitor of ATP citrate lyase, markedly reduced tritiated water incorporation into fatty acids by lung tissue slices. The effects of (-)-hydroxycitrate and n-butymalonate on the incorporation of 14C-labeled glucose, pyruvate, acetate, and citrate suggested that citrate is a major acetyl carrier for de novo fatty acid synthesis in lung tissue. Alternative mechanisms to citrate as an acetyl carrier were also considered. Lung mitochondrial preparations formed significant levels of acetylcarnitine in the presence of pyruvate and carnitine. However, the effect of carnitine on the incorporation of 14C-labeled glucose, pyruvate, acetate, and citrate into fatty acids by lung tissue slices indicated that acetylcarnitine may not be a significant acetyl carrier for fatty acid synthesis but may serve as an acetyl "buffer" in the control of mitochondrial acetyl-CoA levels. Additionally, it appears unlikely that either acetylaspartate or acetoacetate are of major importance in acetyl transfer in lung tissue.

Acetates

Pyruvate metabolism in bovine epididymal spermatozoa.

Treating bovine epididymal spermatozoa with rutamycin or rotenone inhibited both respiration and motility supported by endogenous substrates. When oxidative phosphorylation had been blocked with various inhibitors, pyruvate was metabolized to yield ATP and restored motility. Fructose, which is metabolized via glycolysis to yield ATP, was also able to resuscitate the cells. Other substrates tested (lactate, acetate, alpha-ketoglutarate, or glyoxylate) were unable to restore motility in rutamycin-treated cells. In the presence of pyruvate, the phosphorylation uncoupler, carbonylcyanide-p-trifluoromethyoxphenylhydrazone, reduced motility and ATP to common levels in untreated cells or cells treated with rutamycin or rotenone. Pyruvate is thus metabolized to produce ATP by a pathway independent of oxidative phosphorylation associated with the electron transport chain. 5-Methoxyindole-2-carboxylic acid, an inhibitor of lipoyldehydrogenase, prevented the increase of motility and ATP in rutamycin-treated cells, indicating that alpha-keto acid oxidation is involved in the production of ATP from pyruvate when rutamycin is present. With pyruvate present, bongkrekic acid, antimycin A, and anaerobiosis eliminated motility, reduced ATP to low levels, and also significantly reduced the rate of pyruvate metabolism. Acetate was produced from pyruvate only when cellular ATP concentrations were low. Decreases in free carnitine concentrations showed that pyruvate initially used was converted to acetylcarnitine. The results indicate that the intramitochondrial lactate dehydrogenase X, which is unique to spermatozoa, allows the NADH resulting from pyruvate oxidation to reduce other pyruvate molecules to lactate. Pyruvate thus competes with, and can substitute for, the NADH dehydrogenase of the electron transport chain. Pyruvate rapidly repletes the acetylcarnitine pool under a variety of conditions.

Adenosine Diphosphate

Lipid oxidation by heart mitochondria from young adult and senescent rats.

1. State-3 (i.e. ADP-stimulated) rates of O(2) uptake with palmitoylcarnitine, palmitoyl-CoA plus carnitine, pyruvate plus malonate plus carnitine and octanoate as respiratory substrate were all diminished in heart mitochondria isolated from senescent (24-month-old) rats compared with mitochondria from young adults (6 months old). By contrast, State-3 rates of O(2) uptake with pyruvate plus malate or glutamate plus malate were the same for mitochondria from each age group. 2. Measurements of enzyme activities in disrupted mitochondria showed a decline with senescence in the activity of acyl-CoA synthetase (EC 6.2.1.2 and 6.2.1.3), carnitine acetyltransferase (EC 2.3.1.7) and 3-hydroxy-acyl-CoA dehydrogenase (EC 1.1.1.35), but no change in the activity of carnitine palmitoyltransferase (EC 2.3.1.21) or acyl-CoA dehydrogenase (EC 1.3.99.3). 3. Measurement of dl-[(3)H]carnitine (in)/acetyl-l-carnitine (out) exchange in intact mitochondria showed decreased rates when the animals used were senescent. However, this followed from a decreased intramitochondrial pool of exchangeable carnitine, such that calculated first-order rate constants for exchange were identical in mitochondria from the two age groups. 4. The decline in acyl-CoA synthetase activity is thought to be the reason for the diminished rate of O(2) uptake with octanoate in senescence. The decline in carnitine acetyltransferase activity is considered to be the cause of the diminished rate of O(2) uptake with acetylcarnitine or with pyruvate plus malonate plus carnitine as substrate. The mechanism of the diminished rate of O(2) uptake with palmitoylcarnitine in senescence is discussed.

Acetylcarnitine

Improved radiochemical assay for carnitine and its derivatives in plasma and tissue extracts.

We describe the measurement of carnitine and short-chain and long-chain acylcarnitines in perchloric acid extracts of liver and muscle. [1-14C]Acetyl-CoA is used, and labeled acetylcarnitine is measured with a sensitivity of less than 1 to 50 nmol of L-carnitine per 50-microliter sample. Samples frozen at -20 degrees C lost no carnitine during several months. Analytical recovery of carnitine (5 nmol) added to 50-microliter perchloric acid extracts of liver was 103 +/- 2%. This method may be suitable for clinical applications such as screening patients with muscle and metabolic disorders.

Acetylcarnitine

The effects of clofibrate feeding on the metabolism of palmitate and erucate in isolated hepatocytes.

The metabolism of palmitate and erucate has been investigated in hepatocytes isolated from control rats and from rats fed 0.3% clofibrate. Clofibrate increased the oxidation of [1-14C]palmitate 1.5 to 2-fold while the esterification was decreased. At a high concentration of palmitate (1.5 mM), the total rate of fatty acid metabolism was stimulated. Clofibrate stimulated both the oxidation (3.5 to 5-fold) and the esterfication (1.7-fold) of [14-14C]erucate. Erucate undergoes chain-shortening in isolated liver cells. This chain-shortening was stimulated at least 2-fold by clofibrate feedings. The isolated mitochondrial fraction from clofibrate-fed rats showed an increased capacity for oxidation of short-chain acylcarnitines (including acetylcarnitine), while the oxidation of palmitoyl- and erucoylcarnitine showed little change. It is suggested that erucate is shortened by the recently detected beta-oxidation system of peroxisomes.

Acyltransferases

Effects of rumen fluid transplantation on longissimus dorsi muscle development in Xizang sheep: An association analysis based on transcriptomic and serum metabolomic profiles.

This study aimed to investigate the effects of rumen fluid transplantation (RFT) on the growth and development of the longissimus dorsi muscle in female Xizang sheep. After RFT, muscle lightness differed significantly between the two groups, with the LDC group showing significantly higher lightness than the LDT group. In contrast, no significant differences were observed between groups in other muscle phenotypic traits, including drip loss, pH, cooking loss, shear force, redness, and yellowness. Antioxidant-related indices (SOD, GSH-PX, MDA, CAT, and T-AOC) also showed no significant differences between groups. Histological analysis revealed that muscle fiber length, width, and density were significantly greater in the experimental group than in the control group. Transcriptomic analysis identified 515 differentially expressed genes (DEGs), of which 419 were downregulated. KEGG analysis indicated that genes involved in muscle development-related pathways, such as cell adhesion and the PI3K-Akt signaling pathway, were predominantly downregulated. Key serum metabolites (L-kynurenine, IPA, allantoin, and propionylcarnitine) showed highly significant positive correlations with muscle fiber growth indices. In contrast, metabolites such as l-carnitine, acetylcarnitine, and citrulline were negatively correlated with muscle fiber growth, but positively correlated with the expression of muscle structure-related genes (COL11A1 and EFNA5) and with meat lightness. Overall, this study provides new insights into the potential molecular basis by which RFT influences muscle growth and development. However, the mechanisms by which RFT affects muscle development and meat quality-related traits remain unclear and warrant further investigation.

Animals