D-Carnitine
(Synonyms: 右旋肉碱) 目录号 : GC40661
An isomer of L-carnitine
Cas No.:541-14-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
L-Carnitine is an essential metabolite that has diverse roles in metabolism, most notably facilitating the transport of long-chain fatty acids into the mitochondrial matrix for β-oxidation. L-Carnitine is obtained from dietary sources or by the metabolism of lysine and methioinine. D-Carnitine is an analog of L-carnitine that, in the range of 0.25-1 mM, inhibits the uptake of L-carnitine by cells.
| Cas No. | 541-14-0 | SDF | |
| 别名 | 右旋肉碱 | ||
| Canonical SMILES | [O-]C(C[C@H](O)C[N+](C)(C)C)=O | ||
| 分子式 | C7H15NO3 | 分子量 | 161.2 |
| 溶解度 | Ethanol: 10 mg/ml,PBS (pH 7.2): 10 mg/ml | 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 | 6.2035 mL | 31.0174 mL | 62.0347 mL |
| 5 mM | 1.2407 mL | 6.2035 mL | 12.4069 mL |
| 10 mM | 0.6203 mL | 3.1017 mL | 6.2035 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。
Uptake of L-carnitine, D-Carnitine and acetyl-L-carnitine by isolated guinea-pig enterocytes
Biochim Biophys Acta 1986 May 29;886(3):425-33.PMID:3708005DOI:10.1016/0167-4889(86)90178-3.
Uptake and metabolism of L-carnitine, D-Carnitine and acetyl-L-carnitine were studied utilizing isolated guinea-pig enterocytes. Uptake of the D- and L-isomers of carnitine was temperature dependent. Uptake of L-[14C]carnitine by jejunal cells was sodium dependent since replacement by lithium, potassium or choline greatly reduced uptake. L- and D-Carnitine developed intracellular to extracellular concentration gradients for total carnitine (free plus acetylated) of 2.7 and 1.4, respectively. However, acetylation of L-carnitine accounted almost entirely for the difference between uptake of L- and D-Carnitine. About 60% of the intracellular label was acetyl-L-carnitine after 30 min, and the remainder was free L-carnitine. No other products were observed. D-Carnitine was not metabolized. Acetyl-L-carnitine was deacetylated during or immediately after uptake into intestinal cells and a portion of this newly formed intracellular free carnitine was apparently reacetylated. L-Carnitine and D-Carnitine transport (after adjustment for metabolism and diffusion) were evaluated over a concentration range of 2-1000 microM. Km values of 6-7 microM and 5 microM, were estimated for L- and D-Carnitine, respectively. Ileal-cell uptake was about half that found for jejunal cells, but the labeled intracellular acetylcarnitine-to-carnitine ratios were similar for both cell populations. Carnitine transport by guinea-pig enterocytes demonstrate characteristics of a carrier-mediated process since it was inhibited by D-Carnitine and trimethylaminobutyrate, as well as being temperature and concentration dependent. The process appears to be facilitated diffusion rather than active transport since L-carnitine did not develop a significant concentration gradient, and was unaffected by ouabain or actinomycin A.
Absorption of D- and L-carnitine by the intestine and kidney tubule in the rat
Biochim Biophys Acta 1984 May 16;772(2):209-19.PMID:6722145DOI:10.1016/0005-2736(84)90046-4.
The process by which L- and D-Carnitine are absorbed was investigated using the live rat and the isolated vascularly perfused intestine. A lumenal dose of 2-6 nmol in the perfused intestine resulted in less than 5% transport of either isomer to the perfusate in 30 min. The L-isomer was taken up by the intestinal tissue about twice as rapidly as the D-isomer by both the perfused intestine (52.8% and 21.6%, respectively) and the live animal (80% and 50%, respectively) in 30 min. After 1 h 90% of the L-carnitine had accumulated in the intestinal tissue and was released to the circulation over the next several hours. Accumulation of D-Carnitine reached a maximum of 80% in 2 h and release to the circulations was similar to that of L-carnitine. Uptake of both L-[14C]carnitine and acetyl-L-[14C]carnitine was more rapid in the upper jejunal segment than in other portions of the small intestine. Acetylation occurred in all segments, resulting in nearly 50% conversion to this derivative in 5 min. Increasing the dose of L-carnitine reduced the percent acetylation. The uptake of both isomers was a saturable process and high concentrations of D-Carnitine, acetyl-L-carnitine and trimethylaminobutyrate inhibited L-carnitine uptake. In the live animal after 5 h, the distribution of isotope from L-[14C]carnitine and D-[3H]carnitine differed primarily in the muscle where 29.5% of the L-carnitine and 5.3% of the D-Carnitine was found and in the urine where 2.9% of the L-carnitine and 7.1% of the D-Carnitine was found. The renal threshold for L-carnitine was 80 microM and for D-Carnitine 30 microM, in the isolated perfused kidney. Approx. 40% of the L-carnitine but none of the D-Carnitine excreted in the urine was acetylated. L-Carnitine and D-Carnitine competed for tubular reabsorption.
Comparison of the effects of L-carnitine, D-Carnitine and acetyl-L-carnitine on the neurotoxicity of ammonia
Biochem Pharmacol 1993 Jul 6;46(1):159-64.PMID:8347126DOI:10.1016/0006-2952(93)90360-9.
Although L-carnitine has been reported to have protective effects against ammonia toxicity, conflicting results have also been presented and the mechanisms underlying the protection, if any, are not clear. In the present study, we examined the effects of L-carnitine, D-Carnitine and acetyl-L-carnitine on the neurotoxicity of ammonia. Administration of ammonium acetate (15 mmol/kg) to mice caused seizures, elevation of blood ammonia and urea concentrations, and marked alterations of brain energy metabolites. Pretreatment with either L-carnitine, D-Carnitine or acetyl-L-carnitine reduced the frequency of the seizures, prolonged the time until the first fit, lowered the levels of ammonia in the blood and brain, and suppressed the alterations of brain energy metabolites caused by hyperammonemia. there was no significant difference between L- and D-Carnitine in the potency to inhibit the seizures. In addition, there was no difference between the two chemicals in the potency to decrease the ammonia contents in the blood and brain, or to suppress the alterations of energy metabolites in the brain. When compared with L-carnitine, however, acetyl-L-carnitine better preserved ATP in the brain, while it lowered ammonia in the blood and brain less markedly. These results show that L-carnitine and its analogues do have the potential to suppress the neurotoxicity of ammonia. Moreover, the results suggest that the protective effects of carnitine against the toxicity of ammonia are systemic, that the action of acetyl-L-carnitine may differ from that of L- or D-Carnitine, and that the "classical" function of carnitine is not the sole mechanism underlying the suppression of the neurotoxicity of ammonia.
Chiral Luminescent Sensor Eu-BTB@D-Carnitine Applied in the Highly Effective Ratiometric Sensing of Curing Drugs and Biomarkers for Diabetes and Hypertension
Inorg Chem 2022 Oct 10;61(40):15921-15935.PMID:36170648DOI:10.1021/acs.inorgchem.2c02126.
Chiral drugs are of great significance in drug development and life science because one pair of enantiomers has a different combination mode with target biological active sites, leading to a vast difference in physical activity. Metal-organic framework (MOF)-based chiral hybrid materials with specific chiral sites have excellent applications in the highly effective sensing of drug enantiomers. Sitagliptin and clonidine are effective curing drugs for controlling diabetes and hypertension, while insulin and norepinephrine are the biomarkers of these two diseases. Excessive use of sitagliptin and clonidine can cause side effects such as stomach pain, nausea, and headaches. Herein, through post-synthetic strategy, MOF-based chiral hybrid material Eu-BTB@D-Carnitine (H3BTB = 1,3,5-benzenetrisbenzoic acid) was synthesized. Eu-BTB@D-Carnitine has dual emission peaks at 417 and 616 nm when excited at 330 nm. Eu-BTB@D-Carnitine can be applied in luminescent recognition toward sitagliptin and clonidine with high sensitivity and low detection limit (for sitagliptin detection, Ksv is 7.43 × 106 [M-1]; for clonidine detection, Ksv is 9.09 × 106 [M-1]; limit of detection (LOD) for sitagliptin is 10.21 nM, and LOD of clonidine is 8.34 nM). In addition, Eu-BTB@D-Carnitine can further realize highly sensitive detection of insulin in human fluids with a high Ksv (2.08 × 106 [M-1]) and a low LOD (15.48 nM). On the other hand, norepinephrine also can be successfully discriminated by the hybrid luminescent platform of Eu-BTB@D-Carnitine and clonidine with a high Ksv value of 4.79 × 106 [M-1] and a low LOD of 8.37 nM. As a result, the chiral hybrid material Eu-BTB@D-Carnitine can be successfully applied in the highly effective ratiometric sensing of curing drugs and biomarkers for diabetes and hypertension.
Functional differences between l- and D-Carnitine in metabolic regulation evaluated using a low-carnitine Nile tilapia model
Br J Nutr 2019 Sep 28;122(6):625-638.PMID:32124711DOI:10.1017/S000711451900148X.
l-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.