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Donisi, Isabella, Anna Balestrieri, Vitale Del Vecchio, et al. "l-Carnitine and Acetyl-l-Carnitine Induce Metabolism Alteration and Mitophagy-Related Cell Death in Colorectal Cancer Cells." Nutrients 17, no. 6 (2025): 1010. https://doi.org/10.3390/nu17061010.
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Background/Objectives: Colorectal cancer (CRC) remains one of the most common and deadly malignancies worldwide, driven by metabolic reprogramming and mitochondrial dysfunction, which support tumor growth and progression. Several studies showed that nutrition is a contributing factor in the prevention and management of CRC. In this context, carnitines, amino acid derivatives abundant in food of animal origin, such as meat and milk, are crucial for mitochondrial function. Recently, l-carnitine and acetyl-l-carnitine have received particular attention due to their antioxidant, anti-inflammatory, and antitumor properties. However, to date, there is no conclusive evidence on the effects of l-carnitine and acetyl-l-carnitine in CRC or the underlying molecular mechanism. Methods: In this study, we investigated in HCT 116 and HT-29 CRC cells the effects of l-carnitine and acetyl-l-carnitine on mitochondrial homeostasis by XF HS Seahorse Bioanalyzer and cell death pathways by flow cytometry and western blot assays. Results: Data showed that l-carnitine and acetyl-l-carnitine reduced cell viability (p < 0.001), modulated cellular bioenergetics, and induced oxidative stress (p < 0.001). These phenomena promoted autophagic flux and the mitophagy process via PINK1 and Parkin modulation after 72 h of treatment. Of note, the combined treatment with l-carnitine and acetyl-l-carnitine showed a synergistic effect and enhanced the effect of single carnitines on tumor cell growth and metabolic dysfunction (p < 0.05). Moreover, exposure to l-carnitine and acetyl-l-carnitine promoted CRC cell apoptosis, suggesting a mechanism involving mitophagy-related cell death. These data were associated with increased SIRT4 expression levels (p < 0.01) and the activation of AMPK signaling (p < 0.01). Conclusions: Overall, the results, by supporting the importance of nutritional factors in CRC management, highlight l-carnitine and acetyl-l-carnitine as promising agents to target CRC metabolic vulnerabilities.
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Chen, Zhangwei, Danbo Lu, Baoling Qi, et al. "Quantitative Profiling of Serum Carnitines Facilitates the Etiology Diagnosis and Prognosis Prediction in Heart Failure." Molecules 28, no. 14 (2023): 5345. http://dx.doi.org/10.3390/molecules28145345.
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Background: The perturbation of fatty acid metabolism in heart failure (HF) has been a critical issue. It is unclear whether the amounts of circulating carnitines will benefit primary etiology diagnosis and prognostic prediction in HF. This study was designed to assess the diagnostic and prognostic values of serum carnitine profiles between ischemic and non-ischemic derived heart failure. Methods: HF patients (non-ischemic dilated cardiomyopathy: DCM-HF, n = 98; ischemic heart disease: IHD-HF, n = 63) and control individuals (n = 48) were enrolled consecutively. The serum carnitines were quantitatively measured using the UHPLC-MS/MS method. All patients underwent a median follow-up of 28.3 months. Multivariate Cox regression analysis was performed during the prognosis evaluation. Results: Amongst 25 carnitines measured, all of them were increased in HF patients, and 20 acylcarnitines were associated with HF diagnosis independently. Seven acylcarnitines were confirmed to increase the probability of DCM diagnosis independently. The addition of isobutyryl-L-carnitine and stearoyl-L-carnitine to conventional clinical factors significantly improved the area under the receiver operating characteristic curve (ROC) from 0.771 to 0.832 (p = 0.023) for DCM-HF diagnosis (calibration test for the composite model: Hosmer-Lemeshow χ2 = 7.376, p = 0.497 > 0.05). Using a multivariate COX survival analysis adjusted with clinical factors simultaneously, oleoyl L-carnitine >300 nmol/L (HR = 2.364, 95% CI = 1.122–4.976, p = 0.024) and isovaleryl-L-carnitine <100 nmol/L (HR = 2.108, 95% CI = 1.091–4.074, p = 0.026) increased the prediction of all-cause mortality independently, while linoleoyl-L-carnitine >420 nmol/L, succinyl carnitine >60 nmol/L and isovaleryl-L-carnitine <100 nmol/L increased the risk of HF rehospitalization independently. Conclusions: Serum carnitines could not only serve as diagnostic and predictive biomarkers in HF but also benefit the identification of HF primary etiology and prognosis.
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Placidi, Martina, Teresa Vergara, Giovanni Casoli, et al. "Acyl-Carnitines Exert Positive Effects on Mitochondrial Activity under Oxidative Stress in Mouse Oocytes: A Potential Mechanism Underlying Carnitine Efficacy on PCOS." Biomedicines 11, no. 9 (2023): 2474. http://dx.doi.org/10.3390/biomedicines11092474.
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Carnitines play a key physiological role in oocyte metabolism and redox homeostasis. In clinical and animal studies, carnitine administration alleviated metabolic and reproductive dysfunction associated with polycystic ovarian syndrome (PCOS). Oxidative stress (OS) at systemic, intraovarian, and intrafollicular levels is one of the main factors involved in the pathogenesis of PCOS. We investigated the ability of different acyl-carnitines to act at the oocyte level by counteracting the effects of OS on carnitine shuttle system and mitochondrial activity in mouse oocytes. Germinal vesicle (GV) oocytes were exposed to hydrogen peroxide and propionyl-l-carnitine (PLC) alone or in association with l-carnitine (LC) and acetyl-l-carnitine (ALC) under different conditions. Expression of carnitine palmitoyltransferase-1 (Cpt1) was monitored by RT-PCR. In in vitro matured oocytes, metaphase II (MII) apparatus was assessed by immunofluorescence. Oocyte mitochondrial respiration was evaluated by Seahorse Cell Mito Stress Test. We found that Cpt1a and Cpt1c isoforms increased under prooxidant conditions. PLC alone significantly improved meiosis completion and oocyte quality with a synergistic effect when combined with LC + ALC. Acyl-carnitines prevented Cpt1c increased expression, modifications of oocyte respiration, and ATP production observed upon OS. Specific effects of PLC on spare respiratory capacity were observed. Therefore, carnitine supplementation modulated the intramitochondrial transfer of fatty acids with positive effects on mitochondrial activity under OS. This knowledge contributes to defining molecular mechanism underlying carnitine efficacy on PCOS.
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Di Emidio, Giovanna, Francesco Rea, Martina Placidi, et al. "Regulatory Functions of L-Carnitine, Acetyl, and Propionyl L-Carnitine in a PCOS Mouse Model: Focus on Antioxidant/Antiglycative Molecular Pathways in the Ovarian Microenvironment." Antioxidants 9, no. 9 (2020): 867. http://dx.doi.org/10.3390/antiox9090867.
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Polycystic ovary syndrome (PCOS) is a complex metabolic disorder associated with female infertility. Based on energy and antioxidant regulatory functions of carnitines, we investigated whether acyl-L-carnitines improve PCOS phenotype in a mouse model induced by dehydroepiandrosterone (DHEA). CD1 mice received DHEA for 20 days along with two different carnitine formulations: one containing L-carnitine (LC) and acetyl-L-carnitine (ALC), and the other one containing also propionyl-L-carnitine (PLC). We evaluated estrous cyclicity, testosterone level, ovarian follicle health, ovulation rate and oocyte quality, collagen deposition, lipid droplets, and 17ß-HSD IV (17 beta-hydroxysteroid dehydrogenase type IV) expression. Moreover, we analyzed protein expression of SIRT1, SIRT3, SOD2 (superoxide dismutase 2), mitochondrial transcriptional factor A (mtTFA), RAGE (receptor for AGEs), GLO2 (glyoxalase 2) and ovarian accumulation of MG-AGEs (advanced glycation end-products formed by methylglyoxal). Both carnitine formulations ameliorated ovarian PCOS phenotype and positively modulated antioxidant molecular pathways in the ovarian microenvironment. Addition of PLC to LC-ALC formulation mitigated intraovarian MG-AGE accumulation and increased mtTFA expression. In conclusion, our study supports the hypothesis that oral administration of acyl-L-carnitines alleviates ovarian dysfunctions associated with this syndrome and that co-administration of PLC provides better activity. Molecular mechanisms underlying these effects include anti-oxidant/glycative activity and potentiation of mitochondria.
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Placidi, Martina, Giovanna Di Emidio, Ashraf Virmani, et al. "Carnitines as Mitochondrial Modulators of Oocyte and Embryo Bioenergetics." Antioxidants 11, no. 4 (2022): 745. http://dx.doi.org/10.3390/antiox11040745.
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Recently, the importance of bioenergetics in the reproductive process has emerged. For its energetic demand, the oocyte relies on numerous mitochondria, whose activity increases during embryo development under a fine regulation to limit ROS production. Healthy oocyte mitochondria require a balance of pyruvate and fatty acid oxidation. Transport of activated fatty acids into mitochondria requires carnitine. In this regard, the interest in the role of carnitines as mitochondrial modulators in oocyte and embryos is increasing. Carnitine pool includes the un-esterified l-carnitine (LC) and carnitine esters, such as acetyl-l-carnitine (ALC) and propionyl-l-carnitine (PLC). In this review, carnitine medium supplementation for counteracting energetic and redox unbalance during in vitro culture and cryopreservation is reported. Although most studies have focused on LC, there is new evidence that the addition of ALC and/or PLC may boost LC effects. Pathways activated by carnitines include antiapoptotic, antiglycative, antioxidant, and antiinflammatory signaling. Nevertheless, the potential of carnitine to improve energetic metabolism and oocyte and embryo competence remains poorly investigated. The importance of carnitine as a mitochondrial modulator may suggest that this molecule may exert a beneficial role in ovarian disfunctions associated with metabolic and mitochondrial alterations, including PCOS and reproductive aging.
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Takahashi, M., S. Ueda, H. Misaki, et al. "Carnitine determination by an enzymatic cycling method with carnitine dehydrogenase." Clinical Chemistry 40, no. 5 (1994): 817–21. http://dx.doi.org/10.1093/clinchem/40.5.817.
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Abstract We describe a highly sensitive and specific method for determining L-carnitine in serum by use of carnitine dehydrogenase (EC 1.1.1.108). The method involves a new enzymatic cycling technique with NADH, thio-NAD+, and carnitine dehydrogenase, and measures the increase of absorbance at 415 nm of thio-NADH produced at 37 degrees C during the reaction: [formula: see text] The calibration curve for L-carnitine in serum was linear between 5 and 250 mumol/L. Analytical recovery was 96.5-106%, and within-run and between-run imprecisions (CV) were 0.66-4.33% and 1.02-2.56%, respectively. This method was free from interference by bilirubin, hemoglobin, various acyl-DL-carnitines, and ascorbate. The procedure is simple, rapid, accurate, and automatable. The amount of free L-carnitine in serum (53.6 +/- 11.7 mumol/L, n = 200) was greater in men than in women (45.1 +/- 14.2 mumol/L, n = 200) (mean +/- SD).
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Reuter, Stephanie E., Allan M. Evans, Donald H. Chace, and Gianfranco Fornasini. "Determination of the reference range of endogenous plasma carnitines in healthy adults." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 45, no. 6 (2008): 585–92. http://dx.doi.org/10.1258/acb.2008.008045.
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Background l-carnitine is an endogenous substance, vital in the transport of fatty acids across the inner mitochondrial membrane for oxidation. Disturbances in carnitine homeostasis can have a significant impact on human health; therefore, it is critical to define normal endogenous concentrations for l-carnitine and its esters to facilitate the diagnosis of carnitine deficiency disorders. This study was conducted to determine the normal concentrations of a number of carnitines in healthy adults using three analytical methods. The impact of age and gender on carnitine concentrations was also examined. Methods Blood samples were collected from 60 healthy subjects of both genders and various ages. Plasma samples were analysed for endogenous carnitine concentrations by radioenzymatic assay, high-performance liquid chromatography and electrospray tandem mass spectrometry. Results Precision and accuracy of results obtained for each assay were within acceptable limits. Average endogenous concentrations obtained from the three analytical methods in this study were in the range of 38–44, 6–7 and 49–50 μmol/L for l-carnitine, acetyl-l-carnitine and total carnitine, respectively. Comparison of results between the genders indicated that males had significantly higher endogenous plasma l-carnitine and total carnitine concentrations than females. Age was found to have no impact on plasma carnitine concentrations. Conclusion These results are useful in the evaluation of biochemical or metabolic disturbances and in the diagnosis and treatment of patients with carnitine deficiency.
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Lisboa, Fernando, Lorenzo Segabinazzi, Felipe Hartwig, Camila Freitas-Dell`Aqua, Frederico Papa, and José Dell`Aqua Jr. "L-carnitine and acetyl-L-carnitine enhance stallion sperm quality during semen storage at 5°C." Clinical Theriogenology 14, no. 4 (2022): 339–47. http://dx.doi.org/10.58292/ct.v14i4.9169.
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Carnitine, a powerful antioxidant, has an essential role in sperm energy metabolism. Among carnitines, only L-carnitine’s effect on stallion semen has been tested and not acetyl-L-Carnitine. Therefore, we aimed to determine the ideal concentrations of L-carnitine (LC) and acetyl-L-carnitine (AC) and their effects on stallion semen cooled at 5℃ for up to 48 hours. Semen was extended to 50 x 106 sperm/ml in commercial extender (Control), and concentrations of 5, 10, and 15 mmol/l of LC and AC were evaluated in Experiment 1. Sperm motility and plasma membrane integrity were assessed by CASA and epifluorescence microscopy, respectively. In Experiment 2, the combination of the intermediate doses of LC (10 mmol/l) and AC (10 mmol/l) was tested. Sperm parameters were evaluated as in Experiment 1 and in addition, DNA fragmentation index (DFI), production of reactive oxygen species (ROS), and lipid peroxidation (PEROX) were evaluated by flow cytometry. All analyses were performed at 0, 24, and 48 hours after semen collection, processing, and cooled-stored at 5°C. In Experiments 1 and 2, the groups supplemented with LC and AC or LC+AC had higher plasma membrane integrity and motility parameters compared to Control group (p < 0.05). The LC and AC combination did not change sperm parameters compared to LC or AC alone (p > 0.05). No differences (p > 0.05) were observed for DFI, ROS, and PEROX. In conclusion, LC and AC’s addition, alone or in combination, enhanced sperm motility and plasma membrane integrity of stallion sperm after cooled-storage at 5℃ for up to 48 hours.
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Matsumoto, K., Y. Yamada, M. Takahashi, et al. "Fluorometric determination of carnitine in serum with immobilized carnitine dehydrogenase and diaphorase." Clinical Chemistry 36, no. 12 (1990): 2072–76. http://dx.doi.org/10.1093/clinchem/36.12.2072.
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Abstract A fluorometric flow-injection method for determining carnitine with use of immobilized enzymes carnitine dehydrogenase (EC 1.1.1.108) and diaphorase (EC 1.8.1.4) was developed and applied to the assay of carnitine in serum of patients treated with valproic acid. After fractionation and hydrolysis of carnitines in serum samples by perchloric acid and potassium hydroxide, liberated carnitine was converted to resorufin by immobilized carnitine dehydrogenase and diaphorase in the presence of beta-NAD+ (1.0 mmol/L), resazurin (12.5 mumol/L), and Tris acetate (0.6 mol/L, pH 9.0) at 37 degrees C. The fluorescence intensity of resorufin was monitored at lambda Ex 560 nm and lambda Em 580 nm. The calibration curve was linear for carnitine amounts from 0.1 to 1.0 nmol. Quantitative analytical recovery and satisfactory within- and between-run imprecision of carnitine in each carnitine fraction were obtained. Interference by bilirubin, serum albumin, and hemoglobin was negligible. Carnitine deficiencies were detected in about 20% of the valproic acid-treated patients (n = 198). The present method should be useful for monitoring carnitine deficiencies in clinical laboratories.
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Goa, Karen L., and Rex N. Brogden. "l-Carnitine." Drugs 34, no. 1 (1987): 1–24. http://dx.doi.org/10.2165/00003495-198734010-00001.
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Walter, J. H. "L-Carnitine." Archives of Disease in Childhood 74, no. 6 (1996): 475–78. http://dx.doi.org/10.1136/adc.74.6.475.
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Sulkers, E. J., H. N. Lafeber, J. B. V. Goudoever, et al. "L-carnitine." Lancet 335, no. 8699 (1990): 1215. http://dx.doi.org/10.1016/0140-6736(90)92730-6.
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Eder, Klaus, Juliane Felgner, Karin Becker, and Holger Kluge. "Free and Total Carnitine Concentrations in Pig Plasma after Oral Ingestion of Various L-Carnitine Compounds." International Journal for Vitamin and Nutrition Research 75, no. 1 (2005): 3–9. http://dx.doi.org/10.1024/0300-9831.75.1.3.
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This study was undertaken to investigate the bioavailability of various L-carnitine esters (acetyl-L-carnitine and lauroyl-L-carnitine) and salts (L-carnitine L-tartrate, L-carnitine fumarate, L-carnitine magnesium citrate) relative to base of free L-carnitine. Six groups of five or six piglets each were administered orally a single dose of 40 mg L-carnitine equivalents/kg body weight of each of those L-carnitine compounds. A seventh group served as a control. Free and total plasma carnitine concentrations were determined 1, 2, 3.5, 7, 24, and 32 hours after administration of the single dose. Area-under-the-curve (AUC) values were calculated to assess the bioavailability of the L-carnitine compounds. AUC values, calculated for the time interval between 0 and 32 hours, for both free and total carnitine were similar for base of free L-carnitine and the three L-carnitine salts (L-carnitine L-tartrate, L-carnitine fumarate, L-carnitine magnesium citrate) while those of the two esters (acetyl-L-carnitine, lauroyl-L-carnitine) were lower. Administration of L-carnitine L-tartrate yielded a higher plasma free carnitine AUC value for the time interval between 0 and 3.5 hours than administration of the other compounds. The data of this study suggest that L-carnitine salts have a similar bioavailability to that of free L-carnitine while L-carnitine esters have a lower one. The study also suggests that L-carnitine L-tartrate is absorbed faster than the other L-carnitine compounds.
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Melegh, Béla, László Szücs, János Kerner, and Attila Sándor. "Changes of Plasma Free Amino Acids and Renal Clearances of Carnitines in Premature Infants During L‐Carnitine‐Supplemented Human Milk Feeding." Journal of Pediatric Gastroenterology and Nutrition 7, no. 3 (1988): 424–29. http://dx.doi.org/10.1002/j.1536-4801.1988.tb09559.x.
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SummaryEighteen breast‐fed infants with a mean postnatal age of 26 days (range 16–41 days) were studied. Following 1 control day, the infants were fed for 7 consecutive days with pooled human milk supplemented with 300 nmol L‐carnitine/ml milk. Both plasma fractions of acid‐soluble carnitines increased as a consequence of carnitine application. The level of β‐hydroxybutyrate also increased significantly. Of the circulating free amino acids, the levels of alanine (p < 0.025) and glutamine (p < 0.01) were found to be lower, with a decreased urea level (p < 0.005) by the last day of carnitine administration, compared with the control day. The urinary output of total nitrogen also decreased. There were no statistically significant changes in the level of free fatty acids and glucose. On the control day, the renal clearance rate of esterified carnitines significantly exceeded that of free fraction, thus the relative renal reabsorption calculated on the base of creatinine excretion rates was higher for free (mean 98.1%) than for acylated (mean 90.6%) carnitine. In response to enhanced carnitine intake, the clearance rates for each fractions of carnitines significantly exceeded the presupplementary values. The increased clearance rates was more pronounced for free (mean 13.2‐fold) than for esterified (mean 8.08‐fold) carnitines. Despite the increased clearance rates, considerable relative reabsorption was seen for free carnitines (mean 70.0%) as well as for acylcarnitines (mean 65.3%).
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Demarquoy, Jean. "Revisiting the Role of Carnitine in Heart Disease Through the Lens of the Gut Microbiota." Nutrients 16, no. 23 (2024): 4244. https://doi.org/10.3390/nu16234244.
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L-Carnitine, sourced from red meat, dairy, and endogenous synthesis, plays a vital role in fatty acid metabolism and energy production. While beneficial for cardiovascular, muscular, and neural health, its interaction with the gut microbiota and conversion into trimethylamine (TMA) and trimethylamine N-oxide (TMAO) raise concerns about heart health. TMAO, produced through the gut-microbial metabolism of L-carnitine and subsequent liver oxidation, is associated with cardiovascular risks, including atherosclerosis, heart attacks, and stroke. It contributes to cholesterol deposition, vascular dysfunction, and platelet aggregation. Omnivorous diets, rich in L-carnitine, are associated with higher TMAO levels compared to plant-based diets, which are linked to lower cardiovascular disease risks. Dietary interventions, such as increasing fiber, polyphenols, and probiotics, can modulate the gut microbiota to reduce TMAO production. These strategies seek to balance L-carnitine’s benefits with its potential risks related to TMAO production. Future research should focus on personalized approaches to optimize L-carnitine use while mitigating its cardiovascular impacts, exploring microbial modulation and dietary strategies to minimize the TMAO levels and associated risks.
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Chatzidimitriou, Christos, Theodoros Pliakogiannis, Athanasios Evangeliou, Theodora Tsalkidou, Hans Josef Böhles, and Kleonikos Kalaitzidis. "Evaluation of Carnitine Levels According to the Peritoneal Equilibration Test in Patients on Continuous Ambulatory Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 13, no. 2_suppl (1993): 444–47. http://dx.doi.org/10.1177/089686089301302s112.
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The evidence of carnitine abnormal metabolism in patients on continuous ambulatory peritoneal dialysis (CAPO) is unclear, and previous studies have reported conflicting results. The total (TC), free (FC), and acylated (AC) carnitines were estimated in blood and dialysate, as well as the AC/FC ratio, in 29 patients on CAPO, grouped into high (H-Abs) and low (L-Abs) absorbers, according to the results of the peritoneal equilibration test (fast PE-test). Ourdata demonstrated that patients with higher peritoneal transport rates, which was the H-Abs group, males and females, showed a better carnitine metabolic status compared to the L-Abs group. Although the H-Abs group lost significantly more free carnitine than the L-Abs group, the AC/FC ratio of the H-Abs group remained within normal range. All the patients in our study showed abnormally high triglyceride (TAG) levels and an abnormally high total cholesterol/HOL cholesterol ratio. In particular, the patients In the L-Abs group showed significantly higher TAG levels and total cholesterol/HOL cholesterol ratios than the H-Abs group. Those patients who have been on CAPO for more than 2 years showed significantly abnormally higher AC/FC ratios than those with shorter periods on CAPO treatment. In patients with AC/FC ratio greater than 0.4, the supplementation of L-carnitine may have a beneficial effect on their carnitine and lipid metabolism.
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Hefni, Mohammed E., and Cornelia M. Witthöft. "Development and Application of a UPLC–MRM–MS Method for Quantifying Trimethylamine, Trimethylamine-N-Oxide, and Related Metabolites in Individuals with and Without Metabolic Syndrome." Separations 12, no. 2 (2025): 53. https://doi.org/10.3390/separations12020053.
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Trimethylamine-N-oxide (TMAO) is associated with various chronic diseases. TMAO is a downstream oxidative metabolite of trimethylamine (TMA) that is generated by the gut microbiota from dietary choline, carnitine, and betaine. Current analytical methods predominantly target TMAO only, due to the challenge of efficiently extracting and quantifying TMA. The present study demonstrates a simple and rapid UPLC–MRM–MS method for concurrent quantification of TMAO, TMA, and related precursors (choline, betaine, and various carnitines) following a methanol extraction from plasma and derivatization using iodoacetonitrile (IACN). Pure methanol resulted in a higher extractability of TMA (up to two-fold) compared to both pure acetonitrile and various methanol/acetonitrile mixtures. The quantification method showed high linearity within the tested range of 0.0625–100 μmol/L (determination coefficient > 0.999) and an intra- (n = 3) and inter-day (n = 9) precision of 2–8% along with an average recovery of above 94% for all metabolites (TMAO, TMA, choline, betaine, L-carnitine, acetyl-L-carnitine, and propionyl-L-carnitine). The method’s applicability was confirmed through a comparison of TMAO and its precursor concentrations in plasma samples of overnight-fasted subjects with (n = 12) and without (n = 21) metabolic syndrome.
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Cao, Yu, Yun-xiao Wang, Cheng-juan Liu, Le-xin Wang, Zhi-wu Han, and Chun-bo Wang. "Comparison of pharmacokinetics of L-carnitine, Acetyl-L-carnitine and Propionyl-Lcarnitine after single oral administration of L-carnitine in healthy volunteers." Clinical & Investigative Medicine 32, no. 1 (2009): 13. http://dx.doi.org/10.25011/cim.v32i1.5082.
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Purpose: To investigate the pharmacokinetics of L-carnitine (LC) and its analogues, acetyl-L-carnitine (ALC) and propionyl -L-carnitine (PLC) in healthy volunteers after single L-carnitine administration. Methods: Liquid L-carnitine (2.0 g) was administered orally as a single dose in 12 healthy subjects. Plasma and urine concentrations of L-carnitine, ALC and PLC were detected by HPLC. Results: The maximum plasma concentration (Cmax) and area under the curve (AUC0-?) of L-carnitine was 84.7±25.2 ?mol·L-1·h and 2676.4±708.3 ?mol·L-1·h, respectively. The elimination half-life of L-carnitine and the time required to reach the Cmax (Tmax) was 60.3±15.0 and 3.4±0.46 h, respectively. The Cmax of ALC (12.9±5.5 ?mol·L-1) and PLC (5.08±3.08 ?mol·L-1) was lower than L-carnitine (P < 0.01), so as the AUC0-? (166.2±77.4 and 155.6±264.2?mol·L-1·h, respectively, P < 0.01). The half-life of ALC (35.9±28.9h) and PLC (25.7±30.3 h) was also shorter than L-carnitine (P < 0.01). The 24h accumulated urinary excretion of L-carnitine, ALC and PLC were 613.5±161.7, 368.3±134.8 and 61.3±37.8?mol, respectively. Conclusion: L-carnitine has a greater maximum plasma concentration than ALC and PLC. L-carnitine also has a longer half-life than ALC and PLC. These data may have important implications in the designing of dosing regimens for L-carnitine or its analogues, such as ALC or PLC.
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Iliceto, Mario, Jorunn M. Andersen, Mette Haug Stensen, Trine B. Haugen, and Oliwia Witczak. "Association of Endogenous Seminal L-Carnitine Levels with Post-Thaw Semen Parameters in Humans." Andrologia 2024 (March 1, 2024): 1–11. http://dx.doi.org/10.1155/2024/4327010.
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Cryopreservation of semen is a useful tool for male fertility preservation. Some evidence for a beneficial effect of L-carnitine supplementation of freezing media on cryopreserved semen samples has been reported. Here, we examined the association of endogenous levels of seminal L-carnitine with post-thaw semen parameters. We also investigated the effect of freezing medium supplemented with L-carnitine on sperm characteristics, related to endogenous seminal L-carnitine levels. Semen analyses were performed on 125 fresh samples, and after standard cryopreservation and with L-carnitine as a supplement. Participants were categorized into two groups based on the median levels of endogenous seminal L-carnitine: low L-carnitine (≤38.8 µg/ml) and high L-carnitine (>38.8 µg/ml). After standard cryopreservation, semen samples with high L-carnitine levels showed higher rapid progressive, progressive and total sperm motility and a reduced seminal static oxidation–reduction potential (ORP) level than samples with low L-carnitine levels. Only in post-thaw samples with low L-carnitine levels, there was an increase in the amount of sperm neck midpiece defects, compared to the fresh samples. Cryopreservation with L-carnitine had the most beneficial effect on rapid progressive sperm motility in samples with high endogenous L-carnitine levels. In conclusion, L-carnitine has a beneficial impact on sperm characteristics in post-thaw samples both as an endogenous component in seminal plasma and as a supplement in the freezing medium, by improving sperm motility and reducing seminal oxidative stress.
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Wong, Gail K., and Mark W. Crawford. "Carnitine Deficiency Increases Susceptibility to Bupivacaine-induced Cardiotoxicity in Rats." Anesthesiology 114, no. 6 (2011): 1417–24. http://dx.doi.org/10.1097/aln.0b013e31821a8d46.
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Background Anecdotal reports suggest that carnitine deficiency increases susceptibility to bupivacaine-induced cardiotoxicity. Bupivacaine inhibits lipid-based respiration in myocardial mitochondria via inhibition of acylcarnitine exchange in rats. The authors hypothesized that carnitine deficiency increases susceptibility to bupivacaine-induced asystole in rats and that acute repletion with L-carnitine reverses this effect. Methods Thirty male Sprague-Dawley rats were assigned to three groups. Rats assigned to the L-carnitine-deficient and L-carnitine-replete groups received subcutaneous D-carnitine on the 10 d before the experiment to induce L-carnitine deficiency. Control rats received an equal volume of subcutaneous normal saline. The rats were anesthetized and mechanically ventilated. Bupivacaine was infused intravenously at a rate of 2.0 mg · kg⁻¹ · min⁻¹ until asystole occurred. The L-carnitine-replete group received intravenous L-carnitine 100 mg · kg⁻¹ immediately before bupivacaine infusion. At asystole, blood was sampled to measure bupivacaine concentration. The primary outcome was time to asystole. Results L-carnitine deficiency significantly decreased survival duration (P &lt; 0.0001). Time to bupivacaine-induced asystole decreased by 22% (P &lt; 0.05) in the L-carnitine-deficient group (847 s [787-898]) (median [interquartile range]) compared with controls (1,082 s [969-1,427]). Intravenous administration of L-carnitine completely reversed the reduction in time to asystole. At asystole, the median plasma bupivacaine concentration in the L-carnitine-deficient group was 38% (P &lt; 0.05) less than that in control animals. Plasma bupivacaine concentration was similar in L-carnitine-replete and control animals. Conclusions Carnitine deficiency increased sensitivity to bupivacaine-induced asystole, an effect that was reversed completely by L-carnitine repletion. This study suggests that carnitine deficiency may predispose to bupivacaine-induced cardiotoxicity. L-carnitine may have a protective role against bupivacaine cardiotoxicity.
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Bruzell, Ellen, Berit Granum, Ragna Hetland, et al. "Risk Assessment of "Other Substances" – L-Carnitine and L-Carnitine-L-tartrate." European Journal of Nutrition & Food Safety 8, no. 4 (2018): 174–76. http://dx.doi.org/10.9734/ejnfs/2018/42545.
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Wiseman, Lynda R., and Rex N. Brogden. "Propionyl-L-Carnitine." Drugs & Aging 12, no. 3 (1998): 243–48. http://dx.doi.org/10.2165/00002512-199812030-00006.
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Hiatt, William R. "Propionyl-L-Carnitine." Drugs & Aging 12, no. 3 (1998): 0003–249. http://dx.doi.org/10.2165/00002512-199812030-00007.
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Brevetti, Gregorio. "Propionyl-L-Carnitine." Drugs & Aging 12, no. 3 (1998): 0003–249. http://dx.doi.org/10.2165/00002512-199812030-00008.
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Hart, Andrew M., Andrew DH Wilson, Cristina Montovani, et al. "Acetyl-l-carnitine." AIDS 18, no. 11 (2004): 1549–60. http://dx.doi.org/10.1097/01.aids.0000131354.14408.fb.
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Kraemer, William J., Jeff S. Volek, and Courtenay Dunn-Lewis. "L-Carnitine Supplementation." Current Sports Medicine Reports 7, no. 4 (2008): 218–23. http://dx.doi.org/10.1249/jsr.0b013e318180735c.
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Novak, Milan, Ellen F. Monkus, Maria Buch, John Silverio, Ofelia M. Clouston, and Janet C. Cassady. "L‐Carnitine Supplementation of a Soybean‐Based Formula in Early Infancy." Journal of Pediatric Gastroenterology and Nutrition 7, no. 2 (1988): 220–24. http://dx.doi.org/10.1002/j.1536-4801.1988.tb09509.x.
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SummaryThe absence of carnitine in the diet of normal infants results in marked reduction of plasma carnitine levels. In order to evaluate the effects of L‐carnitine supplementation of soybean formula, plasma and urine levels of free carnitine and acylcarnitine were compared in infants receiving carnitine‐free soybean protein‐based formula and the same formula supplemented with 50 and 250 nmol/ml L‐carnitine. In infants receiving soybean formula with 50 nmol/ml L‐carnitine, the plasma levels of free carnitine were not significantly different from those in infants receiving formula with 250 nmol/ml L‐carnitine; however, urine levels of free carnitine were significantly increased when the infants received formula with 250 nmol/ml L‐carnitine. In normal full‐term infants, supplementation of soybean formula with 50 nmol/ml L‐carnitine was sufficient to maintain normal plasma levels that were comparable to breast‐fed infants.
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Akhoondzadeh, Hamid, Mehrdad Bouyeh, Erwin Paz, Alireza Seidavi, and Radoslava Vlčková. "The effect of dietary L-carnitine and fat on performance, carcass traits and blood components in broiler chickens." Animal Science Papers and Reports 41, no. 2 (2023): 111–22. http://dx.doi.org/10.2478/aspr-2023-0002.
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Abstract The poultry industry has traditionally been selecting animals for improved performance without consideration for the effect on fat deposition. Dietary L-carnitine can alter lipid metabolism; nevertheless, when combined with fat, the effects are not clear. This study shows the effect of different dietary levels of L-carnitine (0, 200 and 400 mg/kg) and fat (0, 2.5 and 5%) on growth performance and slaughter traits of commercial broilers (Ross 308; n=270). The groups received the following dietary treatments: 1) 0 mg/kg L-carnitine + 0% fat, 2) 200 mg/kg L-carnitine + 0% fat, 3) 400 mg/kg L-carnitine + 0% fat, 4) 0 mg/kg L-carnitine + 2.5% fat, 5) 200 mg/kg L-carnitine + 2.5% fat, 6) 400 mg/kg L-carnitine + 2.5% fat, 7) 0 mg/kg L-carnitine + 5.0% fat, 8) 200 mg/kg L-carnitine + 5.0% fat, and 9) 400 mg/kg L-carnitine + 5.0% fat. Feed conversion ratio, growth performance, blood biochemical parameters, carcass traits and body composition were measured and analyzed. Levels of fat with L-carnitine had significant effects on the European Performance Efficiency Factor, wings weight, intestine length and weight, spleen and liver weight, full abdomen carcass and abdominal fat weight, as well as serum triglyceride levels. Dietary L-carnitine supplementation improved growth performance of broilers, thus it may be a promising solution to reduce fat storage in broilers and improve the quality of carcasses intended for human consumption.
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Li, Jia-Min, Ling-Yu Li, Yu-Xue Zhang, et al. "Functional differences between l- and d-carnitine in metabolic regulation evaluated using a low-carnitine Nile tilapia model." British Journal of Nutrition 122, no. 6 (2019): 625–38. http://dx.doi.org/10.1017/s000711451900148x.
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Abstractl-Carnitine is essential for mitochondrial β-oxidation and has been used as a lipid-lowering feed additive in humans and farmed animals. d-Carnitine is an optical isomer of l-carnitine and dl-carnitine has been widely used in animal feeds. However, the functional differences between l- and d-carnitine are difficult to study because of the endogenous l-carnitine background. In the present study, we developed a low-carnitine Nile tilapia model by treating fish with a carnitine synthesis inhibitor, and used this model to investigate the functional differences between l- and d-carnitine in nutrient metabolism in fish. l- or d-carnitine (0·4 g/kg diet) was fed to the low-carnitine tilapia for 6 weeks. l-Carnitine feeding increased the acyl-carnitine concentration from 3522 to 10 822 ng/g and alleviated the lipid deposition from 15·89 to 11·97 % in the liver of low-carnitine tilapia. However, as compared with l-carnitine group, d-carnitine feeding reduced the acyl-carnitine concentration from 10 822 to 5482 ng/g, and increased lipid deposition from 11·97 to 20·21 % and the mRNA expression of the genes involved in β-oxidation and detoxification in the liver. d-Carnitine feeding also induced hepatic inflammation, oxidative stress and apoptosis. A metabolomic investigation further showed that d-carnitine feeding increased glycolysis, protein metabolism and activity of the tricarboxylic acid cycle and oxidative phosphorylation. Thus, l-carnitine can be physiologically utilised in fish, whereas d-carnitine is metabolised as a xenobiotic and induces lipotoxicity. d-Carnitine-fed fish demonstrates increases in peroxisomal β-oxidation, glycolysis and amino acid degradation to maintain energy homeostasis. Therefore, d-carnitine is not recommended for use in farmed animals.
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Garrelds, Ingrid M., Graham R. Elliott, Freek J. Zijlstra, and Iván L. Bonta. "Effects of short- and long-term feeding of L-carnitine and congeners on the production of eicosanoids from rat peritoneal leucocytes." British Journal of Nutrition 72, no. 5 (1994): 785–93. http://dx.doi.org/10.1079/bjn19940080.
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The effect of short- and long-term feeding with L-carnitine, L-acetyl carnitine and L-propionyl carnitine on the production of eicosanoids front in vitro stimulated carrageenan-induced rat peritoneal macrophages was investigated. Both young (4 weeks) and old (18 months) rats were used. A lower number of cells was isolated from the peritonea of treated than control young rats after 4 d feeding, but after 60 d no differences were observed. A similar reduction in cell number was found when old animals were given L-acetyl carnitine or L-propionyl carnitine (acutely) or L-acetyl carnitine or L-carnitine (chronically). Plasma carnitine levels were higher in young rats given carnitine both chronically and acutely. Carnitine derivatives were without effect. In contrast, levels of total carnitine in the plasma of old rats given L-carnitine and L-acetyl carnitine for 4 d and 60 d were higher than in controls. There was no correlation between total plasma carnitine level and effects on prostaglandin, thromboxane and leukotriene B4 (LTB4) production. In young rats the most important changes were observed in relation to the production of prostacyclin (PGI2), measured as 6 keto-prostaglandin Flα. Prostacyclin production was higher in the groups given carnitine or its derivatives. The net result of the changes in PGI2 was that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin Flα:LTB4 ratios tended to be higher in cells from young animals following short-term feeding with L-carnitine. When young rats were given carnitine compounds for 60 d PGI2 production was lower in cells from L-acetyl carnitine- and L-propionyl carnitine-fed animals. The net result of the changes in PGI2 was that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin F1α:LTB4 ratios were lower in cells from animals fed with carnitine compounds. In old rats the PGI2 production was lower after short-term feeding with carnitine compounds and was higher after long-term feeding. LTB4 production was lower after L-carnitine and L-acetyl carnitine treatment for 4 d and also lower after 60 d treatment with L-acetyl carnitine. The net results of the changes in PGI2 were that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin F1α:LTB4 ratios were lower after short-term feeding of all three compounds and higher after the long-term treatment with L-acetyl carnitine and L-propionyl carnitine in old rats. By long-term treatment with low-dose aspirin of patients with heart failure and claudication, the 6 keto-prostaglandin F1α: thromboxane B2 ratio is positively increased, which is a beneficial cardioprotective effect. The mechanism of action of carnitine in heart failure and claudication could also be achieved by an increase of this ratio. Our results suggest that elderly patients could be treated chronically by carnitine to obtain this beneficial effect.
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Liu, Xiaotian. "Effects and mechanism of L-Carnitine on weight loss." Theoretical and Natural Science 4, no. 1 (2023): 78–84. http://dx.doi.org/10.54254/2753-8818/4/20220523.
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L-Carnitine, as an essential coenzyme in fat metabolism, can promote the metabolism of human fat, accelerate the burning of fat, and may achieve the desired fat burning slimming effect; This papers studies the effect of L-carnitine on weight loss and the possible side effects it may bring to the human body, explains the weight loss principle and metabolic pathway of L-carnitine from the molecular level, and discusses the relationship between exercise and L-carnitine in combination with metabolism, give the author recommendations for using L-Carnitine. A brief explanation of the current state of development of L-carnitine diet pills (supplements) in the field of health was described. Combined with the comparison and summary of existing databases, it is concluded that L-carnitine alone is not an ideal choice, and L-carnitine alone is used without exercise: For people with normal weight, L-carnitine has no effect on weight loss. Obviously, only overweight, and obese people, taking L-carnitine combined with a lot of training have obvious weight loss effect.
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Di Lisa, F., R. Menabo, R. Barbato, and N. Siliprandi. "Contrasting effects of propionate and propionyl-L-carnitine on energy-linked processes in ischemic hearts." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (1994): H455—H461. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h455.
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Propionyl-L-carnitine, unlike L-carnitine, is known to improve myocardial function and metabolism altered during the course of ischemia-reperfusion. In this study, the effect of propionyl-L-carnitine has been compared with that of propionate and carnitine on the performance of rat hearts perfused with a glucose-containing medium either under normoxia, ischemia, or postischemic reperfusion. In the postischemic phase, contractile parameters were partially restored both in the control and in the propionate plus carnitine-treated hearts, were markedly impaired by propionate, and were fully recovered by propionyl-L-carnitine. In addition, propionyl-L-carnitine, but not propionate, reduced the functional decay of mitochondria prepared from the ischemic hearts. Even in normoxic conditions propionate, unlike propionyl-L-carnitine, caused a drastic reduction of free CoA and L-carnitine. The concomitant increase in lactate production and decrease in ATP content might be explained by the inhibition of pyruvate dehydrogenase caused by the accumulation of propionyl-CoA. Indeed, when pyruvate was the only oxidizable substrate, propionate induced a gradual decrease in developed pressure, which was largely prevented by L-carnitine. The protective effect of propionyl-L-carnitine may be a consequence of the anaplerotic utilization of propionate in the presence of an optimal amount of ATP and free L-carnitine.
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Dawood, Samy A., Ali Alsuheel Asseri, Ayed A. Shati, Refaat A. Eid, Basiouny El-Gamal, and Mohamed Samir A. Zaki. "L-Carnitine Ameliorates Amiodarone-Mediated Alveolar Damage: Oxidative Stress Parameters, Inflammatory Markers, Histological and Ultrastructural Insights." Pharmaceuticals 17, no. 8 (2024): 1004. http://dx.doi.org/10.3390/ph17081004.
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The aim of this study was to assess L-carnitine’s effects on adult male rats’ lung damage brought on by amiodarone, which is a potent antiarrhythmic with limited clinical efficacy due to potentially life-threatening amiodarone-induced lung damage. Because of the resemblance among the structural abnormalities in rats’ lungs that follows amiodarone medication and pulmonary toxicity in human beings, this animal model may be an appropriate example for this disease entity. Amiodarone produced pulmonary toxicity in twenty-four healthy male albino rats (150–180 g) over a period of 6 weeks. Four groups of six rats each were established: control, sham, amiodarone, and L-carnitine plus amiodarone. Histological, ultrastructural, oxidative stress, and inflammatory markers were determined during a 6-week exposure experiment. Amiodarone-induced lung damage in rats may be brought on due to oxidative stress producing significant pulmonary cytotoxicity, as evidenced by the disruption of the mitochondrial structure, severe fibrosis, and inflammatory response of the lung tissue. Lungs already exposed to such harmful effects may be partially protected by the antioxidant L-carnitine. Biochemical markers of lung damage brought on by amiodarone include lung tissue levels of the enzyme’s catalase, superoxide dismutase, and reduced glutathione. The levels of lipid peroxides in lung tissue measured as malondialdehyde increased significantly upon exposure to amiodarone. In addition, the levels of tumor necrosis factor alpha were significantly elevated in response to amiodarone. The effect of L-carnitine on amiodarone-induced pulmonary toxicity was studied in rats. It is interesting to note that the intake of L-carnitine in rats treated with amiodarone partially restored the biochemical and histopathological alterations brought on by amiodarone to their original levels. Tumor necrosis factor alpha levels were significantly reduced upon L-carnitine exposure. These results suggest that L-carnitine can be used to treat amiodarone-induced pulmonary dysfunction.
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Carillo, Maria Rosaria, Carla Bertapelle, Filippo Scialò, et al. "L-Carnitine in Drosophila: A Review." Antioxidants 9, no. 12 (2020): 1310. http://dx.doi.org/10.3390/antiox9121310.
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L-Carnitine is an amino acid derivative that plays a key role in the metabolism of fatty acids, including the shuttling of long-chain fatty acyl CoA to fuel mitochondrial β-oxidation. In addition, L-carnitine reduces oxidative damage and plays an essential role in the maintenance of cellular energy homeostasis. L-carnitine also plays an essential role in the control of cerebral functions, and the aberrant regulation of genes involved in carnitine biosynthesis and mitochondrial carnitine transport in Drosophila models has been linked to neurodegeneration. Drosophila models of neurodegenerative diseases provide a powerful platform to both unravel the molecular pathways that contribute to neurodegeneration and identify potential therapeutic targets. Drosophila can biosynthesize L-carnitine, and its carnitine transport system is similar to the human transport system; moreover, evidence from a defective Drosophila mutant for one of the carnitine shuttle genes supports the hypothesis of the occurrence of β-oxidation in glial cells. Hence, Drosophila models could advance the understanding of the links between L-carnitine and the development of neurodegenerative disorders. This review summarizes the current knowledge on L-carnitine in Drosophila and discusses the role of the L-carnitine pathway in fly models of neurodegeneration.
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Rodrigues, Brian, David Seccombe, and John H. McNeill. "Lack of effect of oral L-carnitine treatment on lipid metabolism and cardiac function in chronically diabetic rats." Canadian Journal of Physiology and Pharmacology 68, no. 12 (1990): 1601–8. http://dx.doi.org/10.1139/y90-244.
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L-Carnitine is necessary for the transfer of long-chain fatty acids into the mitochondrial matrix where energy production occurs. In the absence of L-carnitine, the accumulation of free fatty acids and related intermediates could produce myocardial subcellular alterations and cardiac dysfunction. Diabetic hearts have a deficiency in the total carnitine pool and develop cardiac dysfunction. This suggested that carnitine therapy may ameliorate alteration in cardiac contractile performance seen during diabetes. In this study, heart function was studied in streptozotocin diabetic rats given L-carnitine orally. Oral L-carnitine treatment (50–250 mg∙kg−1∙day−1) of 1- and 3-week diabetic rats increased plasma free and total carnitine and decreased plasma acyl carnitine levels. In both groups, myocardial total carnitine levels were increased. However, L-carnitine (200 mg∙kg−1∙day−1) treatment of diabetic rats for 6 weeks had no effect on plasma carnitine levels. Similarly, plasma lipids remained elevated whereas cardiac function was still depressed. These studies suggest that in the chronically diabetic rat, the route of administration of L-carnitine is an important factor in determining an effect.Key words: L-carnitine, lipid metabolism, cardiac function, diabetic rats.
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Cao, Yu, Chuan-ji Hao, Chen-jing Wang, et al. "Urinary excretion of L-carnitine, acetyl-L-carnitine, propionyl-L-carnitine and their antioxidant activities after single dose administration of L-carnitine in healthy subjects." Brazilian Journal of Pharmaceutical Sciences 49, no. 1 (2013): 185–91. http://dx.doi.org/10.1590/s1984-82502013000100020.
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The urine excretion of L-carnitine (LC), acetyl-L-carnitine (ALC) and propionyl-Lcarnitine (PLC) and their relations with the antioxidant activities are presently unknown. Liquid L-carnitine (2.0 g) was administered orally as a single dose in 12 healthy subjects. Urine concentrations of LC, ALC and PLC were detected by HPLC. Superoxide dismutase (SOD), total antioxidative capacity (T-AOC), malondialdehyde (MDA) and nitrogen monoxidum (NO) activities were measured by spectrophotometric methods. The 0~2 h, 2~4 h, 4~8 h, 8~12 h, 12~24 h excretion of LC was 53.13±31.36 µmol, 166.93±76.87 µmol, 219.92±76.30 µmol, 100.48±23.89 µmol, 72.07±25.77 µmol, respectively. The excretion of ALC was 29.70±14.43 µmol, 80.59±32.70 µmol, 109.85±49.21 µmol, 58.65±18.55 µmol, and 80.43±35.44 µmol, respectively. The urine concentration of PLC was 6.63±4.50 µmol, 15.33±12.59 µmol, 15.46±6.26 µmol, 13.41±11.66 µmol and 9.67±7.92 µmol, respectively. The accumulated excretion rate of LC was 6.1% within 24h after its administration. There was also an increase in urine concentrations of SOD and T-AOC, and a decrease in NO and MDA. A positive correlation was found between urine concentrations of LC and SOD (r = 0.8277) or T-AOC (r = 0.9547), and a negative correlation was found between urine LC excretions and NO (r = -0.8575) or MDA (r = 0.7085). In conclusion, a single oral LC administration let to a gradual increase in urine L-carnitine excretion which was associated with an increase in urine antioxidant enzymes and the total antioxidant capacities. These data may be useful in designing therapeutic regimens of LC or its analogues in the future.
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Lahjouji, Karim, Ihsan Elimrani, Julie Lafond, Line Leduc, Ijaz A. Qureshi, and Grant A. Mitchell. "l-Carnitine transport in human placental brush-border membranes is mediated by the sodium-dependent organic cation transporter OCTN2." American Journal of Physiology-Cell Physiology 287, no. 2 (2004): C263—C269. http://dx.doi.org/10.1152/ajpcell.00333.2003.
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Maternofetal transport of l-carnitine, a molecule that shuttles long-chain fatty acids to the mitochondria for oxidation, is thought to be important in preparing the fetus for its lipid-rich postnatal milk diet. Using brush-border membrane (BBM) vesicles from human term placentas, we showed that l-carnitine uptake was sodium and temperature dependent, showed high affinity for carnitine (apparent Km = 11.09 ± 1.32 μM; Vmax = 41.75 ± 0.94 pmol·mg protein−1·min−1), and was unchanged over the pH range from 5.5 to 8.5. l-Carnitine uptake was inhibited in BBM vesicles by valproate, verapamil, tetraethylammonium, and pyrilamine and by structural analogs of l-carnitine, including d-carnitine, acetyl-d,l-carnitine, and propionyl-, butyryl-, octanoyl-, isovaleryl-, and palmitoyl-l-carnitine. Western blot analysis revealed that OCTN2, a high-affinity, Na+-dependent carnitine transporter, was present in placental BBM but not in isolated basal plasma membrane vesicles. The reported properties of OCTN2 resemble those observed for l-carnitine uptake in placental BBM vesicles, suggesting that OCTN2 may mediate most maternofetal carnitine transport in humans.
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Savic, Dragana, Leanne Hodson, Stefan Neubauer, and Michael Pavlides. "The Importance of the Fatty Acid Transporter L-Carnitine in Non-Alcoholic Fatty Liver Disease (NAFLD)." Nutrients 12, no. 8 (2020): 2178. http://dx.doi.org/10.3390/nu12082178.
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L-carnitine transports fatty acids into the mitochondria for oxidation and also buffers excess acetyl-CoA away from the mitochondria. Thus, L-carnitine may play a key role in maintaining liver function, by its effect on lipid metabolism. The importance of L-carnitine in liver health is supported by the observation that patients with primary carnitine deficiency (PCD) can present with fatty liver disease, which could be due to low levels of intrahepatic and serum levels of L-carnitine. Furthermore, studies suggest that supplementation with L-carnitine may reduce liver fat and the liver enzymes alanine aminotransferase (ALT) and aspartate transaminase (AST) in patients with Non-Alcoholic Fatty Liver Disease (NAFLD). L-carnitine has also been shown to improve insulin sensitivity and elevate pyruvate dehydrogenase (PDH) flux. Studies that show reduced intrahepatic fat and reduced liver enzymes after L-carnitine supplementation suggest that L-carnitine might be a promising supplement to improve or delay the progression of NAFLD.
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Liu, L., D.-M. Zhang, M.-X. Wang, et al. "The adverse effects of long-term l-carnitine supplementation on liver and kidney function in rats." Human & Experimental Toxicology 34, no. 11 (2015): 1148–61. http://dx.doi.org/10.1177/0960327115571767.
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Levo-Carnitine (l-carnitine) is widely used in health and food. This study was to focus on the adverse effects of 8-week oral supplementation of l-carnitine (0.3 and 0.6 g/kg) in female and male Sprague Dawley rats. l-carnitine reduced body and fat weights, as well as serum, liver, and kidney lipid levels in rats. Simultaneously, hepatic fatty acid β-oxidation and lipid synthesis were disturbed in l-carnitine-fed rats. Moreover, l-carnitine accelerated reactive oxygen species production in serum and liver, thereby triggering hepatic NOD-like receptor 3 (NLRP3) inflammasome activation to elevate serum interleukin (IL)-1β and IL-18 levels in rats. Alteration of serum alkaline phosphatase levels further confirmed liver dysfunction in l-carnitine-fed rats. Additionally, l-carnitine may potentially disturb kidney function by altering renal protein levels of rat organic ion transporters. These observations may provide the caution information for the safety of long-term l-carnitine supplementation.
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Kuwasawa-Iwasaki, Masako, Hiroaki Io, Masahiro Muto, et al. "Effects of l-Carnitine Supplementation in Patients Receiving Hemodialysis or Peritoneal Dialysis." Nutrients 12, no. 11 (2020): 3371. http://dx.doi.org/10.3390/nu12113371.
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l-carnitine is an important factor in fatty acid metabolism, and carnitine deficiency is common in dialysis patients. This study evaluated whether l-carnitine supplementation improved muscle spasm, cardiac function, and renal anemia in dialysis patients. Eighty Japanese outpatients (62 hemodialysis (HD) patients and 18 peritoneal dialysis (PD) patients) received oral l-carnitine (600 mg/day) for 12 months; the HD patients further received intravenous l-carnitine injections (1000 mg three times/week) for 12 months, amounting to 24 months of treatment. Muscle spasm incidence was assessed using a questionnaire, and cardiac function was assessed using echocardiography. Baseline free carnitine concentrations were relatively low in patients who underwent dialysis for >4 years. Total carnitine serum concentration, free carnitine, and acylcarnitine significantly increased after oral l-carnitine treatment for 12 months, and after intravenous l-carnitine injection. There was no significant improvement in muscle spasms, although decreased muscle cramping after l-carnitine treatment was reported by 31% of patients who had undergone HD for >4 years. Hemoglobin concentrations increased significantly at 12 and 24 months in the HD group. Therefore, l-carnitine may be effective for reducing muscle cramping and improving hemoglobin levels in dialysis patients, especially those who have been undergoing dialysis for >4 years.
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Bird, M. I., and E. D. Saggerson. "Interacting effects of l-carnitine and malonyl-CoA on rat liver carnitine palmitoyltransferase." Biochemical Journal 230, no. 1 (1985): 161–67. http://dx.doi.org/10.1042/bj2300161.
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Malonyl-CoA significantly increased the Km for L-carnitine of overt carnitine palmitoyltransferase in liver mitochondria from fed rats. This effect was observed when the molar palmitoyl-CoA/albumin concentration ratio was low (0.125-1.0), but not when it was higher (2.0). In the absence of malonyl-CoA, the Km for L-carnitine increased with increasing palmitoyl-CoA/albumin ratios. Malonyl-CoA did not increase the Km for L-carnitine in liver mitochondria from 24h-starved rats or in heart mitochondria from fed animals. The Km for L-carnitine of the latent form of carnitine palmitoyltransferase was 3-4 times that for the overt form of the enzyme. At low ratios of palmitoyl-CoA/albumin (0.5), the concentration of malonyl-CoA causing a 50% inhibition of overt carnitine palmitoyltransferase activity was decreased by 30% when assays with liver mitochondria from fed rats were performed at 100 microM-instead of 400 microM-carnitine. Such a decrease was not observed with liver mitochondria from starved animals. L-Carnitine displaced [14C]malonyl-CoA from liver mitochondrial binding sites. D-Carnitine was without effect. L-Carnitine did not displace [14C]malonyl-CoA from heart mitochondria. It is concluded that, under appropriate conditions, malonyl-CoA may decrease the effectiveness of L-carnitine as a substrate for the enzyme and that L-carnitine may decrease the effectiveness of malonyl-CoA to regulate the enzyme.
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Li, Jinlian, Yanli Zhang, Haiyun Luan, Xuehong Chen, Yantao Han, and Chunbo Wang. "l-carnitine protects human hepatocytes from oxidative stress-induced toxicity through Akt-mediated activation of Nrf2 signaling pathway." Canadian Journal of Physiology and Pharmacology 94, no. 5 (2016): 517–25. http://dx.doi.org/10.1139/cjpp-2015-0305.
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In our previous study, l-carnitine was shown to have cytoprotective effect against hydrogen peroxide (H2O2)-induced injury in human normal HL7702 hepatocytes. The aim of this study was to investigate whether the protective effect of l-carnitine was associated with the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) pathway. Our results showed that pretreatment with l-carnitine augmented Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H2O2-treated HL7702 cells, although l-carnitine treatment alone had no effect on them. Analysis using Nrf2 siRNA demonstrated that Nrf2 activation was involved in l-carnitine-induced HO-1 expression. In addition, l-carnitine-mediated protection against H2O2 toxicity was abrogated by Nrf2 siRNA, indicating the important role of Nrf2 in l-carnitine-induced cytoprotection. Further experiments revealed that l-carnitine pretreatment enhanced the phosphorylation of Akt in H2O2-treated cells. Blocking Akt pathway with inhibitor partly abrogated the protective effect of l-carnitine. Moreover, our finding demonstrated that the induction of Nrf2 translocation and HO-1 expression by l-carnitine directly correlated with the Akt pathway because Akt inhibitor showed inhibitory effects on the Nrf2 translocation and HO-1 expression. Altogether, these results demonstrate that l-carnitine protects HL7702 cells against H2O2-induced cell damage through Akt-mediated activation of Nrf2 signaling pathway.
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Gross, Carol J., LaVell M. Henderson, and Dennis A. Savaiano. "Uptake of l-carnitine, d-carnitine and acetyl-l-carnitine by isolated guinea-pig enterocytes." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 886, no. 3 (1986): 425–33. http://dx.doi.org/10.1016/0167-4889(86)90178-3.
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Shennan, D. B. "Hyposmotically-Activated Efflux of L-Carnitine from a Human Mammary Cancer Cell Line." Bioscience Reports 21, no. 6 (2001): 779–87. http://dx.doi.org/10.1023/a:1015584724234.
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Cell-swelling, induced by a hyposmotic challenge, stimulated the efflux of L-carnitine from a human mammary cancer cell line, MDA-MB-231. The response was dependent upon the extent of the osmotic shock. Hyposmotically-activated L-carnitine efflux was inhibited by the anion transport blocker diiodosalicylate. The efflux of taurine from MDA-MB-231 cells was also stimulated by a hyposmotic shock via a pathway sensitive to diiodosalicylate. L-carnitine efflux from MDA-MB-231 cells was stimulated by isosmotic swelling in a manner which was inhibited by diiodosalicylate. The results suggest that L-carnitine may exit cells via a volume-sensitive pathway: it is possible that L-carnitine efflux may utilize the same pathway as amino acids. The efflux of L-carnitine via this route could have a major effect on the intracellular concentration of L-carnitine and could facilitate transepithelial L-carnitine transport.
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Antari, Ni Wayan Sukma, and Ida Ayu Manik Damayanti. "UJI EFEKTIVITAS L-CARNITINE TERHADAP KUALITAS SPERMATOZOA PADA MENCIT JANTAN (Mus musculus) YANG DIBERI PAKAN TINGGI LEMAK." Jurnal Riset Kesehatan Nasional 4, no. 2 (2020): 27. http://dx.doi.org/10.37294/jrkn.v4i2.242.
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Penelitian ini bertujuan untuk mengetahui peningkatan kualitas spermatozoa dan hormon testosteron setelah pemberian L-carnitine terhadap pada Mencit Jantan (Mus musculus) Penelitian ini dilakukan dengan memberikan L-carnitine sebagai perlakuan selama 42 hari pada Mencit Jantan dengan variasi dosis 100 mg/kg bb, 150 mg/kg bb dan 200 mg/kg bb dan menggunakan kontrol sebagai pembanding. Variabel yang diamati pada penelitian ini adalah kualitas spermatozoa yaitu: morfologi, motilitas, viabilitas, integritas membrane dan melihat kadar hormone testosteron. Data hasil penelitian diolah menggunakan program statistik komputer (SPSS 22.0 for Windows) dengan menggunakan uji One Way Anova. Hasil penelitian menunjukkan bahwa pemberian suplemen L-carnitin dengan dosis tinggi dalam jangka waktu yang lama dapat menyebabkan menurunnya kualitas spermatozoa yaitu: morfologi, motilitas, viabilitas, dan integritas membran
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De Rubeis, Mariacarla, Ilaria Antenisca Mascitti, Domenica Cocciolone, et al. "Morphological and Redox/Glycative Alterations in the PCOS Oviducts: Modulating Effects of Carnitines in PCOS Mice." Biology 13, no. 12 (2024): 964. http://dx.doi.org/10.3390/biology13120964.
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Polycystic ovarian syndrome (PCOS) is a heterogeneous condition characterized by hyperandrogenism (HA), polycystic ovaries, and dysfunctional ovulation, and it is associated with metabolic problems such as insulin resistance (IR) and obesity. After having investigated the morphological and antioxidant/antiglycative alterations on mouse ovaries and uteri, we here focus on PCOS oviducts, a tract of the reproductive system essential for the nourishment and transport of gametes and embryos. The modulating effects of L-carnitine (LC) and acetyl-L-carnitine (ALC) were also assessed. CD1 mice were administered or not with dehydroepiandrosterone (DHEA, 6 mg/100 g body weight) for 20 days, alone or with 0.40 mg of L-carnitine (LC) and 0.20 mg of acetyl-L-carnitine (ALC). Oviducts were then subjected to histology and immunohistochemistry to evaluate their morphology and collagen deposition, and steroidogenesis. Oxidative, mitochondrial, and methylglyoxal (MG)-dependent damage was also investigated. Transmission electron microscopy was used to detect ultrastructural alterations. The PCOS oviducts were affected by hyperfibrosis, hyperplasia, hypertrophy, and altered steroidogenesis, with oxidative alterations associated with MethylGlyoxal-Advanced Glycation End product (MG-AGE) accumulation. A reduced ciliary coverage and numerous dilated intercellular spaces were found in the epithelium. LC-ALC administration mitigated PCOS oviductal alterations. These results provide evidence for the detrimental action of oxidative and glycative stress in PCOS oviducts, confirming a protective role of carnitines on the PCOS phenotype.
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Berardi, S., B. Hagenbuch, E. Carafoli, and S. Krähenbühl. "Characterization of the endogenous carnitine transport and expression of a rat renal Na+-dependent carnitine transport system in Xenopus laevis oocytes." Biochemical Journal 309, no. 2 (1995): 389–93. http://dx.doi.org/10.1042/bj3090389.
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L-Carnitine transport was characterized in Xenopus laevis oocytes before and after injection of mRNA isolated from rat renal cortex. Non-injected oocytes revealed endogenous Na(+)-dependent transport of L-carnitine. After injection of 15 ng of rat kidney mRNA, the Na(+)-dependent L-carnitine transport increased 2-3-fold, reaching maximal activity after 5-6 days. The expressed carnitine transport was maximal at pH 7.5, whereas the endogenous transport showed no clear maximum between pH 6.0 and 8.5. Kinetic analysis revealed apparent Km values for L-carnitine of 66 microM for the endogenous and 149 microM for the expressed transport. Trimethyl-lysine and D-carnitine inhibited both the endogenous and the expressed transport. In contrast, L-acetylcarnitine, L-isovalerylcarnitine, L-palmitoylcarnitine and butyrobetaine inhibited predominantly the expressed transport, whereas glycinebetaine had no inhibitory effect on either transport system. Size-fractionated rat renal-cortex mRNA (median size 2 kb) induced a 3-fold higher L-carnitine transport than did unfractionated mRNA. These studies demonstrate that Xenopus laevis oocytes exhibit Na(+)-dependent L-carnitine transport and provide the basis for expression-cloning of a rat renal Na(+)-dependent L-carnitine transport system.
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Nakamura, Yusuke, Hiroya Iida, Richi Nakatake, et al. "L-Carnitine has a liver-protective effect through inhibition of inducible nitric oxide synthase induction in primary cultured rat hepatocytes." Functional Foods in Health and Disease 8, no. 3 (2018): 212. http://dx.doi.org/10.31989/ffhd.v8i3.417.
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Background: L-Carnitine has protective effects on various injured organs. However, it has not been reported whether L-carnitine influences the induction of inducible nitric oxide synthase (iNOS) expression during inflammation. Nitric oxide (NO) produced by iNOS is an inflammatory indicator in organs which become inflamed, including the liver.Objective: This study aimed to examine whether L-carnitine influences the induction of iNOS gene expression in inflammatory cytokine-stimulated hepatocytes and the mechanisms involved in the action. Methods: L-Carnitine was added into the primary cultures of rat hepatocytes stimulated by interleukin-1β (an in vitro liver injury model). The production of NO and induction of iNOS and its signaling pathway were analyzed.Results: Transfection experiments with iNOS promoter-luciferase constructs revealed how L-carnitine inhibited iNOS mRNA synthesis activity and reduced its stability. In support of this observation, L-carnitine reduced iNOS mRNA and iNOS protein expression levels, resulting in reduced NO production. L-Carnitine blocked two essential pathways for iNOS induction: IκB kinase (IκB degradation/NF-κB activation) and phosphatidylinositol 3-kinase/Akt (type I IL-1 receptor upregulation).Conclusions: L-Carnitine inhibited the induction of inflammatory mediator iNOS, partially through inhibition of NF-κB activation, which demonstrated L-carnitine has protective effects in an in vitro liver injury model. L-Carnitine may have therapeutic potential for organ injuries, including the liver.Keywords: L-carnitine, hepatic encephalopathy, inducible nitric oxide synthase, liver injury, primary cultured hepatocytes, nuclear factor-κB, type I interleukin-1 receptor
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Shaw, Andy, Stewart Jeromson, Kenneth R. Watterson, et al. "Multiple AMPK activators inhibit l-carnitine uptake in C2C12 skeletal muscle myotubes." American Journal of Physiology-Cell Physiology 312, no. 6 (2017): C689—C696. http://dx.doi.org/10.1152/ajpcell.00026.2016.
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Mutations in the gene that encodes the principal l-carnitine transporter, OCTN2, can lead to a reduced intracellular l-carnitine pool and the disease Primary Carnitine Deficiency. l-Carnitine supplementation is used therapeutically to increase intracellular l-carnitine. As AMPK and insulin regulate fat metabolism and substrate uptake, we hypothesized that AMPK-activating compounds and insulin would increase l-carnitine uptake in C2C12 myotubes. The cells express all three OCTN transporters at the mRNA level, and immunohistochemistry confirmed expression at the protein level. Contrary to our hypothesis, despite significant activation of PKB and 2DG uptake, insulin did not increase l-carnitine uptake at 100 nM. However, l-carnitine uptake was modestly increased at a dose of 150 nM insulin. A range of AMPK activators that increase intracellular calcium content [caffeine (10 mM, 5 mM, 1 mM, 0.5 mM), A23187 (10 μM)], inhibit mitochondrial function [sodium azide (75 μM), rotenone (1 μM), berberine (100 μM), DNP (500 μM)], or directly activate AMPK [AICAR (250 μM)] were assessed for their ability to regulate l-carnitine uptake. All compounds tested significantly inhibited l-carnitine uptake. Inhibition by caffeine was not dantrolene (10 μM) sensitive despite dantrolene inhibiting caffeine-mediated calcium release. Saturation curve analysis suggested that caffeine did not competitively inhibit l-carnitine transport. To assess the potential role of AMPK in this process, we assessed the ability of the AMPK inhibitor Compound C (10 μM) to rescue the effect of caffeine. Compound C offered a partial rescue of l-carnitine uptake with 0.5 mM caffeine, suggesting that AMPK may play a role in the inhibitory effects of caffeine. However, caffeine likely inhibits l-carnitine uptake by alternative mechanisms independently of calcium release. PKA activation or direct interference with transporter function may play a role.
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Yuan, Junhua, Qixiao Jiang, Limin Song, et al. "L-Carnitine Is Involved in Hyperbaric Oxygen-Mediated Therapeutic Effects in High Fat Diet-Induced Lipid Metabolism Dysfunction." Molecules 25, no. 1 (2020): 176. http://dx.doi.org/10.3390/molecules25010176.
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Lipid metabolism dysfunction and obesity are serious health issues to human beings. The current study investigated the effects of hyperbaric oxygen (HBO) against high fat diet (HFD)-induced lipid metabolism dysfunction and the roles of L-carnitine. C57/B6 mice were fed with HFD or normal chew diet, with or without HBO treatment. Histopathological methods were used to assess the adipose tissues, serum free fatty acid (FFA) levels were assessed with enzymatic methods, and the endogenous circulation and skeletal muscle L-carnitine levels were assessed with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Additionally, western blotting was used to assess the expression levels of PPARα, CPT1b, pHSL/HSL, and UCP1. HFD treatment increased body/adipose tissue weight, serum FFA levels, circulation L-carnitines and decreased skeletal muscle L-carnitine levels, while HBO treatment alleviated such changes. Moreover, HFD treatment increased fatty acid deposition in adipose tissues and decreased the expression of HSL, while HBO treatment alleviated such changes. Additionally, HFD treatment decreased the expression levels of PPARα and increased those of CPT1b in skeletal muscle, while HBO treatment effectively reverted such changes as well. In brown adipose tissues, HFD increased the expression of UCP1 and the phosphorylation of HSL, which was abolished by HBO treatment as well. In summary, HBO treatment may alleviate HFD-induced fatty acid metabolism dysfunction in C57/B6 mice, which seems to be associated with circulation and skeletal muscle L-carnitine levels and PPARα expression.