• Journal of Nutrition and Health
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• v.40 no.2
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• pp.118-129
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• 2007

This study was performed to investigate the effect of lysine-limited diets containing different levels of L-carnitine on body weight and lipid metabolism in obesity-induced adult rats. Eight-month-old male Sprague-Dawley rats (n = 90) were raised for one month with high fat diet (40% fat as calorie) to induce obesity. After induction of obesity, rats weighing 739.5 g were randomly blocked into three groups according to the body weight and raised for eight weeks with control diet (Co), 50% lysine-limited diet (-L), 50% lysine limitation with 0.3% pivalate diet (-L + P). Each of three groups was allotted to 0.0% L-carnitine (0.0% CT), 0.5% L-carnitine (0.5% CT) and 2.5% L-carnitine (2.5% CT) groups, respectively. The levels of AST, ALT, total protein and albumin in plasma were within the normal range. Daily food intake and calorie intake tended to be lower in 2.5% CT groups than those of other groups regardless lysine limitation or pivalate intake. And body weight gain and calorie efficiency ratio (weight gain (g) /calorie intake (100 kcal)) were significantly the lowest in 2.5% CT groups among all experimental groups regardless of lysine limitation or pivalate intake. The weights of perirenal, epididymal fat pads and brown adipose tissue in 2.5% CT groups were significantly lower than 0.0% CT groups. Plasma total lipid, triglyceride, total cholesterol concentrations in all groups were not significant by experimental compound. HDL-cholesterol concentrations in -L + P +2.5% CT group were highest in -L + P groups. Levels of hepatic total lipid, triglyceride and total cholesterol in 2.5% CT groups were tend to be lower those than in 0.0% CT groups regardless of dietary lysine limitation and pivalate intake. Fecal total lipid excretions of 2.5% CT groups were significantly lower than in 0.0% CT groups in all experimental groups. But fecal triglyceride excretions of 2.5% CT groups were significantly higher than 0.0% CT groups regardless of lysine limitation and pivalate. In conclusion, there was no difference on body weight and lipid metabolism by dietary lysine limitation and pivalate intake. And feeding of 2.5% L-carnitine was more effective than feeding of 0.5% L-carnitine and 0.0% L-carnitine in reduction of body weight, body fat and lipid metabolism.

• Journal of Chest Surgery
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• v.24 no.5
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• pp.429-437
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• 1991

Beta hydroxytrimethylammonium butyrate[L-carnitine] is highly concentrated in myocardium and it is essential substance for transfer of fatty acids into the mitochondria. We respect that L-carnitine has protective action to myocardium during ischemia. I studied coronary flow and CK - MB isoenzyme of coronary effluent of Langendorff`s isolated rat heart model. As a control group 5 Sprague-Dowley species rat hearts were connected to Langendorff`s isolated rat heart model and perfused for 30 minutes with Kreb-Henseleit buffer solution. After cessation of perfusion for 30 minutes they were reperfused for 30 minutes. In experimental group 10 Sprague-Dowley species rat hearts were perfused with 10mmole /L of L-carnitine contained in Kleb-Henseleit buffer solution. In equilibrium state, coronary flow was 1.7 times greater in experimental group. During reperfusion, both group showed equally decreased flow amount of about 60% of that of equilibrium state. CK-MB isoenzyme level of perfused coronary fluid showed no significant difference in equilibrium state. In reperfusion. CK-MB isoenzyme levels of control group were 17.61$\pm$8. 68U/L at 25 minutes, 23.32$\pm$4.15U /L at 30 minutes; and in experimental group, 13.63$\pm$6. 08U/L at 15 minutes and 13.6$\pm$8.41U /L at 30 minutes respectively. Those values in both states showed significantly lower CK-MB level in experimental group. In conclusion, L-carnitine prevent ischemic myocardial damage during ischemic and reperfusion state of Langendorff`s isolated rat hearts and also I suggest the L-carnitine act potent coronary vasodilator during preischemic and postischemic states of rat hearts.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.227.1-227.1
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• 2003

Acetyl-L-carnitine (ALC), an endogenous component of L-Carnitine, is the acetyl ester of carnitine that has been reported to be beneficial in depressive disorders and Alzheimer's disease.ALC is so hygroscopic that deliquescence took place when it absorbed moisture by 15%(w/w) in a week and then reached steady-state at 45%(w/w) in 40$^{\circ}C$, 75% RH storage condition. Therefore it is necessary to prevent ALC from absorbing atmospheric moisture. For this purpose, we chose hydroxypropylmethylcellulose phthalate (HPMCP) an enteric polymer, as a film former. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.217.3-217.3
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• 2003

Acetyl-L-carnitine, a physiological component of the L-carnitine family, has been proposed for treating Alzheimer's disease in pharmacological doses. Acetyl-L-carnitine and d3-acetylcarnitine (internal standard) were analyzed by electrospray ionization / tandem mass spectrometry (ESI/MS/MS) after derivatization to their butylesters through treatment with butanolic hydrogen chloride. Acetyl-L-carnitine produced a protonated precursor ion at m/z 260 and a corresponding product ion of m/z 85. Analytes were separated on a Capcell Pak C18 (2.0${\times}$150mm, 5 mm). (omitted)

• Preventive Nutrition and Food Science
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• v.8 no.2
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• pp.119-123
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• 2003

To investigate the effects of the supplementation of carnitine and/or ${\gamma}$ -aminobutric acid (GABA), Sprague-Dawley male rats were orally treated with either an AIN-76 diet (control), a control diet plus ethanol (CE, 4 g ethanol/kg bw), CE plus L-carnitine (CEC, 0.5 g/kg bw), CE plus GABA (CEG, 0.5 g/kg bw), or CE plus L-carnitine plus GABA (CECG, 0.25 g/kg bw each) for 6 weeks. Serum triglyceride levels were increased in the CE group and were decreased significantly in the CEC, CEG and CECG groups. HDL-cholesterol was increased and LDL-cholesterol was decreased in the CEG and CECG groups compared with the CE group. Serum GOT and GPT levels increased by the chronic ethanol administration were decreased in the CEC group. In addition, we have evaluated the mRNA levels of carnitine palmitoyltransferase-I in those groups. Supplementation of carnitine/GABA had some recovery effects on the liver CPT-I mRNA levels which decreased by chronic ethanol administration. These results may suggest that supplementations of either L-carnitine or GABA aye effective on the recovery of chronic ethanol-related symptoms, but no combined effects were shown.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.2
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• pp.237-242
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• 2001

Colostrum deprived, newborn pigs (N=12, $1.64{\pm}0.05kg$) were used to study the renal threshold of carnitine, and effects of emulsified medium-chain triglyceride (MCT, tri-8:0) feeding on kinetics of plasma carnitine and urinary carnitine excretion. An arterial catheter was inserted through an umbilical artery, and a bladder catheter was inserted via the urachus. Piglets were oro-gastrically gavaged with one of six carnitine levels (0, 60, 120, 180, 240, $480{\mu}mol/kg\;W^{0.75}$) with (+MCT) or without medium-chain triglycerides (-MCT) in 0.9% NaCl solution. Blood was sampled into heparinized tubes at 0, 1, 2, 4, 6, 8, 14, and 20 h after gavage, and urine was collected and pooled into 1 h or 2 h composite samples to determine free- and short-chain carnitine concentrations. Plasma from the 12 newborn piglets before gavage contained $10.6{\pm}1.2{\mu}mol/L$ free carnitine and $7.2{\pm}0.6{\mu}mol/L$ acid-soluble acyl carnitine. The renal threshold for carnitine was similar between the MCT and the +MCT group (42.6 13.1 and $46.4{\pm}2.0{\mu}mol/L$, respectively), but the correlation between plasma free carnitine and urinary excretion was altered. Plasma free carnitine linearly increased with increasing carnitine dosage (-MCT group, $R^2=0.95$, p<0.001; +MCT group, $R^2=0.91$, p<0.001), but was decreased by 50% when medium-chain triglycerides were fed. The peak in plasma free carnitine concentration was depressed by medium-chain triglycerides feeding also. Therefore, the plasma and urinary short-chain/free carnitine ratio of the +MCT group was increased by 100% and 40%, respectively (p<0.01). Feeding of medium-chain triglycerides may delay plasma carnitine elevation via altering the kinetics of absorption. Similarly, the plasma and urinary short-chain/free carnitine ratio were affected by interaction between medium-chain triglycerides and time (p<0.01). The present study suggests that an oral carnitine dose over $480{\mu}mol/kg\;W^{0.75}$ may be needed to reach the free carnitine renal threshold within a short period, especially when provided together with medium-chain triglyceride.

• Food Science of Animal Resources
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• v.34 no.6
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• pp.749-756
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• 2014

A rapid and simple analytical method for L-carnitine was developed for infant and toddler formulas by liquid chromatography tandem mass spectrometry (LC-MS/MS). A 0.3 g of infant formula and toddler formula sample was mixed in a 50 mL conical tube with 9 mL water and 1 mL 0.1 M hydrochloric acid (HCl) to chemical extraction. Then, chloroform was used for removing a lipid fraction. After centrifuged, L-carnitine was separated and quantified using LC-MS/MS with electrospray ionization (ESI) mode. The precursor ion for L-carnitine was m/z 162, and product ions were m/z 103 (quantitative) and m/z 85 (qualitative), respectively. The results for spiked recovery test were in the range of 93.18-95.64% and the result for certified reference material (SRM 1849a) was within the range of the certificated values. This method could be implemented in many laboratories that require time and labor saving.

• Analytical Science and Technology
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• v.18 no.2
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• pp.163-167
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• 2005

In this study, a novel analytical method has been developed for the rapid determination of L-carnitine in human plasma using electrospray ionization tandem mass spectrometry. Free carnitine (FC) was analyzed after extraction with 80% methanol and total carnitine (TC) was analyzed after hydrolysis and extraction. Acyl carnitine (AC) was subtracted FC from TC. Analytical methods used multiple reaction monitoring (MRM) scan modes. A correlation coefficient of linear regression ($r^2$) was 0.9995, recovery was 97%, reproducibility was less than 10%, and limit of detection (LOD) was $0.0016{\mu}mol/L$. This method reduced sample preparation time and showed high resolution and good reproducibility compared to that with liquid chromatographic methods. Normal control showed AC was lower than FC. Clinical management of patients with inborn error of metabolism showed FC was lower than AC. Thus, carnitine fraction level was very important to monitoring patients with metabolic disorder.

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.12
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• pp.1809-1815
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• 2003

A $3{\times}4$ (chromium and L-carnitine) experiment was designed to investigate the single and interactive effects of adding yeast Cr and L-carnitine to corn-soybean meal diets on lipid metabolism of broiler chickens. Four hundred and eighty one-day-old avian chickens were randomly allocated to 12 treatments of 40 each for 7 weeks. Levels of adding Cr were 0, 400, $600{\mu}g/kg$ and those of Lcarnitine was 0, 30, 50, 100 mg/kg, respectively. The result showed that adding $600{\mu}g/kg$ Cr or 100 mg/kg L-carnitine alone had better regulative effects on fat and cholesterol metabolism than lower adding levels. Effects were more significant at the end of the experiment. There were significantly interactive effects between Cr and L-carnitine on triaclyglycerol, whole cholesterol, HDL, dissociating FFA, and blood glucose, cholesterol and triaclyglycerol of liver, and cholesterol of chest muscle at the end of experiment (p=0.0001-0.0315). But Cr or L-carnitine had no significant effect on growth performance of broiler chickens (p>0.05).

• Journal of Nutrition and Health
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• v.36 no.7
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• pp.720-728
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• 2003

This study was conducted to evaluate changes in plasma concentration and urinary excretion of carnitine, as well as plasma lipid level and fatty acid composition, caused by short term supplementation of carnitine in humans. Ten healthy male subjects (21.2 $\pm$ 0.5 years old) received oral carnitine supplementation (4 g/day) as tablets for two weeks. Fasting blood and random urine samples were collected from each subject both prior to and at the end of carnitine supplemention program. Following the 2 weeks of carnitine supplementation, plasma total carnitine (TCNE) concentration increased 20% (85.1 $\pm$ 7.4 vs 67.3 $\pm$ 9.1 $\mu$ mol/1, p> 0.05), while urinary excretion of total carnitine increased ten times compared to the value measured prior to the supplementation (3051 $\pm$ 692 vs 278 $\pm$ 90.1 $\mu$ mol/g creatinine, p < 0.01). Non-esterified carnitine (NEC) comprised from 71 to 88% of TCNE in plasma, and from 32 to 40% of TCNE excreted in the urine. Two weeks of carnitine supplementation in healthy adults significantly elevated plasma level of acid soluble acylcarnitine (ASAC) which is esterified mostly with short chain fatty acids (21.6 $\pm$ 1.6 $\mu$ mol/l) compared to the value measured prior to the supplementation (6.4 $\pm$ 0.8 $\mu$ mol/l) (p < 0.05). Carnitine supplementation significantly increased plasma HDL-cholesterol level (p < 0.05), and decreased the atherogenic index (p < 0.05), but failed to cause any significant change in plasma levels of total cholesterol, triglyceride, and free fatty acids. Plasma triglyceride and phospholipid fatty acid compositions were not significaly affected as well by the oral supplementation of carnitine in subjects with normal range of blood lipid levels.