Oleoylcarnitine
(Synonyms: CAR 18:1, C18:1 Carnitine, L-Carnitine oleoyl ester, L-Oleoylcarnitine) 目录号 : GC38560
A long-chain acylcarnitine
Cas No.:38677-66-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >96.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Oleoyl-L-carnitine is a naturally occurring long-chain acylcarnitine.1 It inhibits lecithin:cholesterol acyltransferase (LCAT) activity in isolated rat, but not human, plasma by 32% when used at a concentration of 500 ?M.
1.Bell, F.P.Carnitine esters: Novel inhibitors of plasma lecithin: Cholesterol acyltransferase in experimental animals but not in man (Homo sapiens)Int. J. Biochem.15(2)133-136(1983)
| Cas No. | 38677-66-6 | SDF | |
| 别名 | CAR 18:1, C18:1 Carnitine, L-Carnitine oleoyl ester, L-Oleoylcarnitine | ||
| Canonical SMILES | CCCCCCCC/C=C\CCCCCCCC(O[C@H](CC([O-])=O)C[N+](C)(C)C)=O | ||
| 分子式 | C25H47NO4 | 分子量 | 425.64 |
| 溶解度 | DMSO : 100 mg/mL (234.94 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3494 mL | 11.747 mL | 23.494 mL |
| 5 mM | 0.4699 mL | 2.3494 mL | 4.6988 mL |
| 10 mM | 0.2349 mL | 1.1747 mL | 2.3494 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
CPT2 downregulation adapts HCC to lipid-rich environment and promotes carcinogenesis via acylcarnitine accumulation in obesity
Gut 2018 Aug;67(8):1493-1504.PMID:29437870DOI:10.1136/gutjnl-2017-315193.
Objective: Metabolic reprogramming of tumour cells that allows for adaptation to their local environment is a hallmark of cancer. Interestingly, obesity-driven and non-alcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (HCC) mouse models commonly exhibit strong steatosis in tumour cells as seen in human steatohepatitic HCC (SH-HCC), which may reflect a characteristic metabolic alteration. Design: Non-tumour and HCC tissues obtained from diethylnitrosamine-injected mice fed either a normal or a high-fat diet (HFD) were subjected to comprehensive metabolome analysis, and the significance of obesity-mediated metabolic alteration in hepatocarcinogenesis was evaluated. Results: The extensive accumulation of acylcarnitine species was seen in HCC tissues and in the serum of HFD-fed mice. A similar increase was found in the serum of patients with NASH-HCC. The accumulation of acylcarnitine could be attributed to the downregulation of carnitine palmitoyltransferase 2 (CPT2), which was also seen in human SH-HCC. CPT2 downregulation induced the suppression of fatty acid β-oxidation, which would account for the steatotic changes in HCC. CPT2 knockdown in HCC cells resulted in their resistance to lipotoxicity by inhibiting the Src-mediated JNK activation. Additionally, Oleoylcarnitine enhanced sphere formation by HCC cells via STAT3 activation, suggesting that acylcarnitine accumulation was a surrogate marker of CPT2 downregulation and directly contributed to hepatocarcinogenesis. HFD feeding and carnitine supplementation synergistically enhanced HCC development accompanied by acylcarnitine accumulation in vivo. Conclusion: In obesity-driven and NASH-driven HCC, metabolic reprogramming mediated by the downregulation of CPT2 enables HCC cells to escape lipotoxicity and promotes hepatocarcinogenesis.
Inhibition of adenine nucleotide translocase by Oleoylcarnitine, oleoylcoa and oleate in isolated arterial mitochondria
Atherosclerosis 1980 Sep;37(1):21-32.PMID:6252909DOI:10.1016/0021-9150(80)90090-8.
Adenine nucleotide translocase (AdNT) activity was studied in isolated mitochondria from normal rabbit aortas. The enzyme was inhibited by oleic acid, oleoylCoA, and Oleoylcarnitine with 50% inhibition occurring at 5 muM, 6 muM and 14 muM, respectively (corresponding to 8, 10, and 23 nmol/mg protein). PalmitoylCoA and palmitoylcarnitine displayed similar potency to oleylCoA and Oleoylcarnitine. The possibility that inhibition by fatty acid, acylCoA, and acylcarnitine could be attributed to non-specific detergency effects seems remote in that these compounds were more potent inhibitors of AdNT than equimolar concentrations of laurylsulfate. In addition, by use of the fluorescent probe N-phenyl-1-naphthylamine, it was shown that under the experimental conditions, inhibition of AdNT occurred at concentrations not exceeding a critical micelle concentration (CMC). Specificity was also suggested in that octanoylCoA was a weak inhibitor of AdNT and acetylcarnitine, butyrylcarnitine, cholesteryl oleate, and sphingomyelin were not inhibitory to the enzyme. In contrast to the observed inhibition of arterial AdNT by oleoylCoA and Oleoylcarnitine, AdNT in isolated rabbit and rat heart mitochondria was inhibited only by oleoylCoA.
Systemic inflammatory markers in patients with polyneuropathies
Front Immunol 2023 Feb 13;14:1067714.PMID:36860843DOI:10.3389/fimmu.2023.1067714.
Introduction: In patients with peripheral neuropathies (PNP), neuropathic pain is present in 50% of the cases, independent of the etiology. The pathophysiology of pain is poorly understood, and inflammatory processes have been found to be involved in neuro-degeneration, -regeneration and pain. While previous studies have found a local upregulation of inflammatory mediators in patients with PNP, there is a high variability described in the cytokines present systemically in sera and cerebrospinal fluid (CSF). We hypothesized that the development of PNP and neuropathic pain is associated with enhanced systemic inflammation. Methods: To test our hypothesis, we performed a comprehensive analysis of the protein, lipid and gene expression of different pro- and anti-inflammatory markers in blood and CSF from patients with PNP and controls. Results: While we found differences between PNP and controls in specific cytokines or lipids, such as CCL2 or Oleoylcarnitine, PNP patients and controls did not present major differences in systemic inflammatory markers in general. IL-10 and CCL2 levels were related to measures of axonal damage and neuropathic pain. Lastly, we describe a strong interaction between inflammation and neurodegeneration at the nerve roots in a specific subgroup of PNP patients with blood-CSF barrier dysfunction. Conclusion: In patients with PNP systemic inflammatory, markers in blood or CSF do not differ from controls in general, but specific cytokines or lipids do. Our findings further highlight the importance of CSF analysis in patients with peripheral neuropathies.
A plasma long-chain acylcarnitine predicts cardiovascular mortality in incident dialysis patients
J Am Heart Assoc 2013 Dec 5;2(6):e000542.PMID:24308938DOI:10.1161/JAHA.113.000542.
Background: The marked excess in cardiovascular mortality that results from uremia remains poorly understood. Methods and results: In 2 independent, nested case-control studies, we applied liquid chromatography-mass spectrometry-based metabolite profiling to plasma obtained from participants of a large cohort of incident hemodialysis patients. First, 100 individuals who died of a cardiovascular cause within 1 year of initiating hemodialysis (cases) were randomly selected along with 100 individuals who survived for at least 1 year (controls), matched for age, sex, and race. Four highly intercorrelated long-chain acylcarnitines achieved the significance threshold adjusted for multiple testing (P<0.0003). Oleoylcarnitine, the long-chain acylcarnitine with the strongest association with cardiovascular mortality in unadjusted analysis, remained associated with 1-year cardiovascular death after multivariable adjustment (odds ratio per SD 2.3 [95% confidence interval, 1.4 to 3.8]; P=0.001). The association between Oleoylcarnitine and 1-year cardiovascular death was then replicated in an independent sample (n=300, odds ratio per SD 1.4 [95% confidence interval, 1.1 to 1.9]; P=0.008). Addition of Oleoylcarnitine to clinical variables improved cardiovascular risk prediction using net reclassification (NRI, 0.38 [95% confidence interval, 0.20 to 0.56]; P<0.0001). In physiologic profiling studies, we demonstrate that the fold change in plasma acylcarnitine levels from the aorta to renal vein and from pre- to posthemodialysis samples exclude renal or dialytic clearance of long-chain acylcarnitines as confounders in our analysis. Conclusions: Our data highlight clinically meaningful alterations in acylcarnitine homeostasis at the time of dialysis initiation, which may represent an early marker, effector, or both of uremic cardiovascular risk.
A Metabolomic Approach in Search of Neurobiomarkers of Perinatal Asphyxia: A Review of the Current Literature
Front Pediatr 2021 Jun 25;9:674585.PMID:34249811DOI:10.3389/fped.2021.674585.
Perinatal asphyxia and the possible sequelae of hypoxic-ischemic encephalopathy (HIE), are associated with high morbidity and mortality rates. The use of therapeutic hypothermia (TH) commencing within the first 6 h of life-currently the only treatment validated for the management of HIE-has been proven to reduce the mortality rate and disability seen at follow up at 18 months. Although there have been attempts to identify neurobiomarkers assessing the severity levels in HIE; none have been validated in clinical use to date, and the lack thereof limits the optimal treatment for these vulnerable infants. Metabolomics is a promising field of the "omics technologies" that may: identify neurobiomarkers, help improve diagnosis, identify patients prone to developing HIE, and potentially improve targeted neuroprotection interventions. This review focuses on the current evidence of metabolomics, a novel tool which may prove to be a useful in the diagnosis, management and treatment options for this multifactorial complex disease. Some of the most promising metabolites analyzed are the group of acylcarnitines: Hydroxybutyrylcarnitine (Malonylcarnitine) [C3-DC (C4-OH)], Tetradecanoylcarnitine [C14], L-Palmitoylcarnitine [C16], Hexadecenoylcarnitine [C16:1], Stearoylcarnitine [C18], and Oleoylcarnitine [C18:1]. A metabolomic "fingerprint" or "index," made up of 4 metabolites (succinate × glycerol/(β-hydroxybutyrate × O-phosphocholine)), seems promising in identifying neonates at risk of developing severe HIE.