Carnitine Status Research Articles

Serum Carnitine Levels in Childhood Leukemia

In patients with malignancies, the system of carnitine seems abnormally expressed. The serum total, free, and acyl carnitine levels in 40 children and adolescents with acute leukemia were determined using electrospray tandem mass spectrometry in 4 different phases of the disease: at the diagnosis, 1 year after the initiation of chemotherapy, at the end of treatment, and 2.4+/-1.668 years after the completion of chemotherapy. The age, sex, hemoglobin values, serum biochemistry, somatometric features of the patients, and the risk group of the disease were examined. Although the carnitine levels were found higher in patients compared with the control group from diagnosis to treatment completion, statistically significant decrease in carnitine levels was observed in patients within different phases of the disease especially during induction and consolidation treatment (phase A to B) for both free and total (P=0.023) carnitine. In addition, a statistically significant recovery in carnitine levels was observed between phase B (end of intensive chemotherapy) and D (some years after the completion of treatment) for free and total carnitine (P=0.054 and 0.035, respectively). No statistical correlation was documented between the carnitine levels and somatometric parameters or other variables studied. In conclusion, a significant transient decrease in the levels of carnitine during the treatment was observed in children with acute leukemia. Further studies are required to clarify the role of carnitine status in patients with malignancies and possibly the necessity of carnitine supplementation during chemotherapy administration.

Effects of in ovo administration of L-carnitine on hatchability performance, glycogen status and insulin-like growth factor-1 of broiler chickens

1. Eggs from a meat-type breeder flock (Ross) were used in two trials to study the effects of in ovo administration of L-carnitine (carnitine) on hatchability traits (hatchability percentage, embryo deaths, pipped with live or dead embryo), chick weight at hatch as an absolute value (CWT) or expressed as a percentage of egg weight (CWT%), hatching period, glycogen status (liver and pectoral muscle) and plasma insulin-like growth factor-1 (IGF-1) of hatched chicks were investigated. There were 9 treatments with three replicates of each. Treatments were non-injected control (negative control), or injection with sterilised saline (0⋅9%, positive control), or sterilised saline with carnitine at 25, 50, 100, 200, 300, 400, and 500 µg/egg. 2. In ovo carnitine treatment increased CWT, CWT%, glycogen in the liver and pectoral muscle, glycogen index and plasma IGF-1 of hatched chicks, and did not influence hatchability traits and hatching period. The glycogen index of hatched chicks of the in ovo carnitine treatments with values (500 > 400 = 300 > 200) was higher than that of the control and in ovo carnitine at 25, 50, and 100 µg/egg treatments. The nature of response to carnitine was cubic for CWT and CWT%, and linear for glycogen in the liver and pectoral muscle, glycogen index of hatched chicks when the negative control or positive control treatment was used as base line. 3. It was concluded that in ovo administration of carnitine at 25–500 µg/egg increased chick weight at hatch and IGF-1, and did not influence hatchability traits and hatching period of eggs. The linear relationship between in ovo administration of carnitine and glycogen status of hatched chicks indicated that increasing in ovo doses improved glycogen status of hatched chicks.

Carnitine in Parenteral Nutrition

Several new functions or metabolic uses of carnitine and improvements in assessment of carnitine status impact carnitine dosing recommendations. Carnitine dosing will likely be customized for patients at different stages of the life cycle and for patients with dysfunction of different organs. Nutrition supplementation of carnitine should be 2-5 mg x kg(-1) x day(-1) and be administrated via the route used for administration of macronutrients. Pharmacologic supplementation of carnitine should be 50-100 mg x kg(-1) x day(-1) and be reserved for the removal of toxic compounds from the body.

Carnitine Insufficiency Caused by Aging and Overnutrition Compromises Mitochondrial Performance and Metabolic Control

In addition to its essential role in permitting mitochondrial import and oxidation of long chain fatty acids, carnitine also functions as an acyl group acceptor that facilitates mitochondrial export of excess carbons in the form of acylcarnitines. Recent evidence suggests carnitine requirements increase under conditions of sustained metabolic stress. Accordingly, we hypothesized that carnitine insufficiency might contribute to mitochondrial dysfunction and obesity-related impairments in glucose tolerance. Consistent with this prediction whole body carnitine diminution was identified as a common feature of insulin-resistant states such as advanced age, genetic diabetes, and diet-induced obesity. In rodents fed a lifelong (12 month) high fat diet, compromised carnitine status corresponded with increased skeletal muscle accumulation of acylcarnitine esters and diminished hepatic expression of carnitine biosynthetic genes. Diminished carnitine reserves in muscle of obese rats was accompanied by marked perturbations in mitochondrial fuel metabolism, including low rates of complete fatty acid oxidation, elevated incomplete beta-oxidation, and impaired substrate switching from fatty acid to pyruvate. These mitochondrial abnormalities were reversed by 8 weeks of oral carnitine supplementation, in concert with increased tissue efflux and urinary excretion of acetylcarnitine and improvement of whole body glucose tolerance. Acetylcarnitine is produced by the mitochondrial matrix enzyme, carnitine acetyltransferase (CrAT). A role for this enzyme in combating glucose intolerance was further supported by the finding that CrAT overexpression in primary human skeletal myocytes increased glucose uptake and attenuated lipid-induced suppression of glucose oxidation. These results implicate carnitine insufficiency and reduced CrAT activity as reversible components of the metabolic syndrome.

Carnitine status of pregnant women: effect of carnitine supplementation and correlation between iron status and plasma carnitine concentration

It has been shown that plasma carnitine concentrations markedly decline during gestation in women. The reason for this, however, is unknown. One objective of this study was to investigate the effect of carnitine supplementation on plasma carnitine concentrations in pregnant women. The second objective was to investigate the hypothesis that reduced plasma carnitine concentrations during gestation are caused by a reduced carnitine synthesis because of a diminished iron status. Healthy pregnant women (n=26) were randomly assigned in two groups receiving either a L-carnitine supplement (500 mg L-carnitine per day as L-carnitine L-tartrate) (n=13) or placebo (n=13) from the 13th week of gestation to term. In the control group, there was a marked reduction of plasma carnitine concentration from the 12th week of gestation to term. This reduction was prevented by the supplementation of carnitine. In the control group, there was a positive relationship between the parameters of iron status (mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and ferritin) and plasma concentration of carnitine (P<0.05). Moreover, there were inverse correlations between the concentrations of ferritin and the carnitine precursor gamma-butyrobetaine in plasma, and between gamma-butyrobetaine and carnitine in plasma (P<0.05). This study confirms that plasma carnitine concentrations decline in the course of pregnancy, an effect that can be prevented by the supplementation of carnitine. Data of this study, moreover, suggest that the decline of plasma carnitine concentration during pregnancy could be caused by a reduced rate of carnitine biosynthesis, possibly because of an inadequate iron status.

The risk of asymptomatic hyperammonemia in children with idiopathic epilepsy treated with valproate: Relationship to blood carnitine status

Valproate (VPA) administration may be associated with adverse metabolic effects, among is hyperammonemia, which could suggest metabolic abnormalities as carnitine deficiency. This study aimed to evaluate the risk frequency of hyperammonemia and abnormal carnitine levels in children receiving VPA who were otherwise free of neurological or obvious nutritional problems. Ammonia levels were prospectively evaluated in 60 epileptic children with primary epilepsy free of neurological or nutritional problems and were treated with VPA for at least 1 year. Forty healthy children were included as controls. Ammonia levels were correlated with total carnitine (TC), free carnitine (FC), acylcarnitine (AC) and AC/FC ratio. The abnormal ammonia and carnitine levels were also re-checked after 3 months treatment with L-carnitine. Compared to pre-treatment and control levels, the mean TC and FC were lower (p<0.001) while ammonia (p<0.01), AC (p<0.05) and AC/FC ratio (p<0.01) were higher. In the treated group of epileptics, TC and FC were negatively associated with ammonia (r=-0.896, p<0.0001; r=-0.935, p<0.0001). Significant associations were found between FC and AC/FC levels and patient's age (FC; r=0.457, p<0.05, AC/FC; r=-0.435, p<0.05) and dose of VPA (FC; r=-0.753, p<0.001, AC/FC; r=0.591, p<0.01). Ammonia was correlated with patients' age (r=-0.532, p<0.01) and dose of VPA (r=0.673, p<0.01). The abnormal ammonia and carnitine levels were returned to normal after L-carnitine supplementation. Epileptic children treated with VPA and free of neurological disabilities are at risk for hyperammonemia that may be associated with hypocarnitinemia. Patients will benefit from early recognition and preventive measures as carnitine supplementation.

Activities of γ-butyrobetaine dioxygenase and concentrations of carnitine in tissues of pigs

In contrast to other species, less is known about carnitine homeostasis in the pig. This study was performed to yield information about the site of carnitine synthesis and carnitine concentrations in various tissues of pigs ( Sus scrofa). We found that among several pig tissues, a considerable activity of γ-butyrobetaine dioxygenase (BBD), the last enzyme of carnitine synthesis, exists, like in humans and several other species, only in liver and kidney. Activity of that enzyme in liver and kidney was lower at birth than in the subsequent weeks of life. Highest carnitine concentrations were found in skeletal muscle and heart. Carnitine concentrations in plasma, liver and kidney at birth were higher than in the subsequent weeks of life in spite of the low BBD activity at birth. In conclusion, this study shows that liver and kidney are the major sites of carnitine synthesis and that neonatal pigs do not have an insufficient carnitine status.

Supplementation of L-carnitine in pigs: Absorption of carnitine and effect on plasma and tissue carnitine concentrations

This study was performed to investigate the bioavailability of carnitine supplements and their effects on the carnitine status of pigs. Seven groups of young pigs with an average body weight of 10 kg were fed a basal diet or the same diets supplemented with 25, 50, 100, 200, 500 or 1000 mg of L-carnitine per kg for 20 days. Absorption rate of the supplemented carnitine in the small intestine, assessed by the use of titanium dioxide as an indigestible indicator, was greater than 95% for the lower doses (25, 50, 100 mg/kg) and greater than 90% for the higher doses (200, 500, 1000 mg/kg). Supplementation of carnitine caused a dose-dependent increase of free carnitine, acetyl and total carnitine concentrations in plasma, liver, kidney, heart and skeletal muscle. At the highest dose of 1000 mg/kg, plasma and tissue total carnitine concentrations were 3- to 6-fold higher than in the unsupplemented control group. In conclusion, the present study shows that young pigs have a high capacity to absorb carnitine from the diet. It is also shown that plasma and tissue carnitine concentrations in young pigs can be markedly increased by supplementation of carnitine.

Maternal Dietary L-Carnitine Supplementation Influences Fetal Carnitine Status and Stimulates Carnitine Palmitoyltransferase and Pyruvate Dehydrogenase Complex Activities in Swine

Effects of increasing maternal L-carnitine on carnitine status and energy metabolism in the fetus were evaluated by feeding pregnant swine a corn-soybean–based diet containing either 0 or 50 mg/kg added L-carnitine (n = 10/treatment) during the first 70 d of gestation. Carnitine, carnitine palmitoyltransferase (CPT), and pyruvate dehydrogenase complex (PDHC) activities were analyzed in tissues collected from fetuses on d 55 and 70. Maternal L-carnitine supplementation increased both fetal free and long-chain carnitine concentrations by 45% in liver and free carnitine by 31% in heart tissues but did not affect kidney tissue. Elevations in free and acylcarnitines increased with gestational age from 55 to 70 d in liver but not in heart and kidney. The increased carnitine concentrations resulted in a 45% increase in PDHC activity in heart and liver on d 70 of gestation but did not affect kidney and liver on d 55 of gestation. The increases in carnitine concentrations were accompanied by a 70% increase in hepatic CPT activity in 70-d-old fetuses, but activities in heart and kidney were unaffected. The Michaelis constant (Km) of CPT for carnitine in fetal tissues was not influenced by carnitine supplementation (P > 0.1). Notably, the concentrations of carnitine measured on d 70 were only 25–40% of the Km values in liver, 60–70% in heart, and 30–40% in kidney (P < 0.001). We conclude that carnitine ingestion during pregnancy increases fetal carnitine concentrations and stimulates heart PDHC and liver CPT activity without altering carnitine Km.

Carnitine Status in Early-Treated Children, Adolescents and Young Adults with Phenylketonuria on Low Phenylalanine Diets

Background: In patients with phenylketonuria (PKU), the carnitine status may be impaired for metabolic or dietary reasons, including low carnitine intake, a deficient synthesis and acylcarnitine production from phenylalanine (Phe) metabolites. Methods: Free carnitine and acylcarnitine status was assessed in 30 PKU patients, aged 0.5–36 years, mean age 13.8 years. Our cohort was divided into 2 groups according to the preparations of Phe-free amino acids (AA) prescribed, with or without carnitine supplementation. Daily Phe intake, dosage of AA mixtures and body weight were recorded along with measurements of acylcarnitines in blood spots (by tandem mass spectrometry) and serum AA. Control data were obtained from 50 healthy volunteers (aged 0.2–39 years, mean age 14.2. years). Statistical analysis comprised the t test, ANOVA and Pearson’s correlation. Results: PKU patients had lower free carnitine (C0) concentrations than controls (25.82 ± 7.38 vs. 31.28 ± 6.17 µmol/l; p < 0.001) and lower octanoyl- and decanoylcarnitine. Mean C0 and acylcarnitine concentrations did not differ between PKU patients taking the various protein substitutes with or without carnitine; mean C0 levels in PKU patients receiving AA enriched with carnitine were still lower compared with controls (p < 0.05). Conclusions: Actual dietary regimens can not completely normalize the carnitine status; therefore, carnitine levels should be given careful consideration in subjects with PKU.

A moderate excess of dietary lysine lowers plasma and tissue carnitine concentrations in pigs

This study was performed to investigate whether dietary lysine concentration influences the carnitine status of pigs. Therefore, an experiment with twenty young pigs with an average body weight of 21 kg was performed which were fed either a control diet (9.7 g lysine/kg) or a diet with a moderate excess of lysine (16.8 g lysine/kg). Concentrations of all the other amino acids did not differ between the diets. Pigs fed the high-lysine diet had lower concentrations of free and total carnitine in plasma, liver, kidney and skeletal muscle than control pigs (P<0.05). Pigs fed the high-lysine diet moreover had an increased concentration of trimethyllysine (TML), a reduced mRNA abundance of TML dioxygenase and reduced concentrations of gamma-butyrobetaine (BB) in muscle, indicating that the conversion of TML into BB in muscle was impaired. Concentrations of BB, the metabolic precursor of carnitine, in plasma, liver and kidney were also reduced in pigs fed the high-lysine diet while the activity of BB dioxygenase in kidney was not different and that in liver was even increased compared to control pigs (P<0.05). In conclusion, this study shows that a moderate dietary excess of lysine lowers plasma and tissue carnitine concentrations in pigs. Reduced concentrations of BB in liver and kidney suggest that the depressed carnitine status was likely caused by a decreased rate of carnitine synthesis due to a diminished availability of carnitine precursor, probably mainly as a result of an impaired BB formation in muscle.

Carnitine compartmentalization in surgery patients

Carnitine, an amino acid derivative, is involved in the transport of fatty acids into the mitochondrial matrix for βoxidation. Plasma carnitine is often used as a clinical indicator of the carnitine status throughout the body, but the carnitine concentration in organs and the relationship of carnitine compartments within the body are usually not known. We measured plasma carnitine collected before (PC) and during anesthesia (Surg‐PC), red blood cell carnitine collected before (RC) and during anesthesia (Surg‐RC), muscle carnitine (MuC) collected during general anesthesia, and in approximately half of the patients liver carnitine (LC) collected during general anesthesia. Total carnitine values of the various compartments are shown in the table below.Surg‐PC was lower than PC (p&lt;.05), but RC and Surg‐RC did not differ. Correlations of MuC or LC with any of the blood carnitine parameters indicated that less than 15 percent of the tissue carnitine concentration could be predicted by the blood carnitine parameters. Neither plasma carnitine nor red blood cell carnitine appears to be a strong predictor of carnitine status in tissue compartments.

Impact of fasting and postprandial state on plasma carnitine concentrations during aerobic exercise in type 2 diabetes

The effects of metabolic states of fasting and post-absorption on plasma concentrations of free carnitine (FC), acylcarnitine (AC) and total carnitine (TC) were compared during submaximal exercise in subjects with type 2 diabetes mellitus. Ten sedentary men (54+/-5 years) treated with oral hypoglycaemic agents were tested on two separate occasions: following an overnight fast and 2 h after a 395-kcal standardised breakfast. Exercise was performed at 60% of [Formula: see text]O(2peak) on a cycle ergometer for 60 min. Blood samples were drawn at rest for baseline values and following 60 min of exercise and 30 min of recovery. Our results show that: (1) baseline levels of TC, FC and AC were similar in fasted and postprandial groups, (2) TC and AC levels were increased during exercise in the fasted group only, (3) FC levels were decreased during exercise in both fasted and postprandial state and (4) the AC/FC ratio increased during exercise in the fasted group. Our results indicate that the metabolic state of the diabetic patient is associated with a different plasma carnitine status. These patterns may reflect differences in energy metabolism associated with fasting and postprandial hyperglycaemia.

Serum carnitine, triglyceride and cholesterol profiles in Korean neonates

This study evaluated carnitine and lipid status of fifty Korean newborns. Each subject was assigned to two groups: one according to body weight at birth and the other according to gestational age. Serum total, HDL- and LDL-cholesterol were significantly lower and triacylglycerols were significantly higher, by 14 %, in the low birth weight infant (LBWI, 1310-2490 g) group compared with the normal birth weight infant (NBWI, 2570-4420 g) group. Neither birth weight nor gestational age affected serum total carnitine concentrations. However, serum ASAC (acid-soluble acylcarnitine) concentrations were 43 % higher (P < 0.001) in the LBWI group compared with the NBWI group, and approximately twice as high (P < 0.05) in the 28-32 gestational age group compared with the other gestational age groups. NEC (non-esterified acyl carnitine) fractions were significantly higher in the NBWI and 28-32 week groups (P < 0.001 and P < 0.05); consequently serum acyl/NEC carnitine ratios were four times higher in the LBWI group compared with the NBWI group and 2-3 times higher in the 25-32 week age group compared with the more advanced gestational age groups. Urinary carnitine excretion, including the NEC fraction and total carnitine, was significantly higher (P < 0.001) for LBWI than for NBWI. By gestational age, NEC excretion of the 28-32 week group was significantly (P < 0.05) higher than that of the other two groups, but total carnitine excretion was not different among the groups. This study demonstrated that Korean immature and preterm newborns have higher serum triacylglycerol concentrations but lower carnitine status than NBWI. Therefore, the lower carnitine status and moderately higher triacylglycerols may suggest that LBWI in Korea might be at risk for poor carnitine status and decreased capacity to utilise fatty acids for energy.

Effect of l-Carnitine Infusion and Feed Restriction on Carnitine Status in Lactating Holstein Cows

Previously we determined that abomasal infusion of l-carnitine increased in vitro hepatic fatty acid oxidation, decreased liver lipid accumulation, and supported higher fat-corrected milk yield in feed-restricted lactating cows. The objectives of this study were to examine the effects of supplemental l-carni-tine and amount of feed intake on free carnitine and carnitine ester concentrations in liver, muscle, milk, and plasma of lactating dairy cows. Eight lactating Holstein cows (132±36 d in milk) were used in a replicated 4×4 Latin square design with 14-d periods to test factorial combinations of water or l-carnitine infusion (20g/d; d 5 to 14) and ad libitum or restricted (50% of previous 5-d intake; d 10 to 14) dry matter intake. Plasma was obtained 3 times daily on d 4, 8, and 12; milk samples were collected on d 8, 9, 13, and 14. Liver and muscle were biopsied on d 14 of each period. Free carnitine, short-chain acylcarnitine, and long-chain acylcarnitine concentrations were determined using a radioenzymatic assay coupled with ion exchange chromatography. Abomasal l-carnitine infusion increased total carnitine in plasma on d 8 and d 12. All liver carnitine fractions were increased by carnitine infusion. Feed restriction elevated concentrations of free carnitine, long-chain acylcarnitine, and total carnitine in liver tissue from carnitine-infused cows but not in those infused with water. In muscle, acid-soluble carnitine, long-chain acylcarnitine, and total carnitine concentrations were increased by carnitine infusion and feed restriction without significant interaction. Feed restriction increased free carnitine concentrations in muscle from water-infused cows but not in carnitine-infused cows. Carnitine infusion increased the concentration of each milk carnitine fraction as well as milk carnitine output on d 8 to 9. On d 13 to 14, all carnitine fractions except short-chain acylcarnitine were increased in milk from water-infused, feed-restricted cows, whereas all fractions were increased in carnitine-infused, feed-restricted cows. Carnitine infusion increased total carnitine in plasma, liver, muscle, and milk during feed restriction, whereas feed restriction alone increased carnitine concentrations in muscle and milk but not in liver. Liver carnitine concentrations might limit hepatic fatty acid oxidation capacity in dairy cows during the periparturient period; therefore, supplemental l-carnitine might decrease liver lipid accumulation in periparturient cows.

Pivalate lowers litter sizes and weights in female rats independent of its effect on carnitine status

The present study investigated whether treatment of female rats with pivalate affects their reproductive function. Therefore, two experiments with female rats were performed. The first experiment included two groups of rats which received drinking water without (control) or with 20 mmol pivalate/L. The second experiment included a control group (which received drinking water without pivalate and a diet without added carnitine) and four groups which received drinking water with 20 mmol/L pivalate and diets without or with 1, 3 or 5 g added carnitine/kg, respectively. In both experiments, rats treated with pivalate had a lower number of pups born alive and, as a consequence of this, lower litter weights than control rats ( p < 0.05); pup weights were not altered by pivalate treatment. Supplementation of dietary carnitine in Experiment 2 increased plasma and tissue carnitine concentration even in excess of those in control rats but did not restore normal litter sizes. This study shows for the first time that pivalate affects the reproductive function in female rats independent of its effect on the carnitine status.

Effects of chemical diabetes and starvation on blood and organ carnitine concentrations in rats

Carnitine (CARN) is known for shuttling fatty acids across the mitochondrial membrane, but its role in carbohydrate (CHO) metabolism is less well defined. This study examines the effect of altered CHO metabolism on CARN status. Agestratified rats received one of the treatments in Table 1. Total CARN was measured in plasma, red blood cells (RBC), liver, heart, muscle, and epididymis. Table 1: Male and Female Carnitine Concentrations

Influences of Short -term Aerobic Exercise and Supplementation of Carnitine With or Without Choline on Body Weight, Serum Leptin and Carnitine as Well as Lipid Status In Male Rats

Background: Carnitine is essential for fatty acids translocation, muscles function and exercise performance. Choline is a lipotropic agent that prevents deposition of fat in the liver. The studies concerning the effects of carnitine and choline supplementation with exercise on carnitine status and serum leptin are rare. The aim of the present study was to study the effect of carnitine and its combination with choline, with or without exercise on body and total fat pad (TFP) weights, serum carnitine, leptin, β-hydroxy butyric acid (β-HBA), triacylglycerols (TAG) and Free Fatty acids (FFA). Also, total lipids (TL) and TAG content of TFP and urinary carnitine were investigated. Material and Methods: 48 male rats were equally divided to the following groups: control (C), carnitine (5 g/Kg diet) supplemented, carnitine plus choline (5 and 11.5 g /Kg diet respectively) supplemented. Half of each group was subjected to short term aerobic exercise on manual treadmill, in which the speed and duration were gradually increased via the course of the experiment, to be 10 m/min for 20 min/day, 5 days/week in the last 2 weeks. Body weights were recorded weekly. After 6 weeks, The 24 hours urine was collected then the fasted rats were sacrificed and blood and the total fat pad (TFP) were collected for analysis. Results: Carnitine supplementation, tended to decrease body weight, TFP, TAG content and serum FFA, and significantly decreased the TL content, serum leptin, TAG (P<0.0005). Carnitine feeding resulted in a significant elevation of serum carnitine, β-HBA and urinary carnitine (P<0.0005), compared to sedentary control rats. These values became more pronounced on choline addition to the diet except for serum and urinary carnitine that reversed (i.e. decreased) by choline addition. Exercise intervention resulted in a significant decrease in body weight, TFP, TL content and serum leptin, TAG and FFA. These values were more pronounced in both supplements with exercise, specially serum carnitine. However, exercise caused reduction of urinary carnitine in non-supplemented and carnitine supplemented groups and this was reversed by choline and exercise. Conclusion: Our study demonstrated that the beneficial effects of carnitine supplements is promoted by choline with or without mild exercise to reduce body weight, body fat, serum leptin and promote fat loss by increasing lipolysis as indicated by increased serum β-HBA. These results may or may not be applicable to humans, so further research is recommended to determine whether similar effects would result in humans or not.

Influences of Short -term Aerobic Exercise and Supplementation of Carnitine With or Without Choline on Body Weight, Serum Leptin and Carnitine as Well as Lipid Status In Male Rats

Background: Carnitine is essential for fatty acids translocation, muscles function and exercise performance. Choline is a lipotropic agent that prevents deposition of fat in the liver. The studies concerning the effects of carnitine and choline supplementation with exercise on carnitine status and serum leptin are rare. The aim of the present study was to study the effect of carnitine and its combination with choline, with or without exercise on body and total fat pad (TFP) weights, serum carnitine, leptin, β-hydroxy butyric acid (β-HBA), triacylglycerols (TAG) and Free Fatty acids (FFA). Also, total lipids (TL) and TAG content of TFP and urinary carnitine were investigated. Material and Methods: 48 male rats were equally divided to the following groups: control (C), carnitine (5 g/Kg diet) supplemented, carnitine plus choline (5 and 11.5 g /Kg diet respectively) supplemented. Half of each group was subjected to short term aerobic exercise on manual treadmill, in which the speed and duration were gradually increased via the course of the experiment, to be 10 m/min for 20 min/day, 5 days/week in the last 2 weeks. Body weights were recorded weekly. After 6 weeks, The 24 hours urine was collected then the fasted rats were sacrificed and blood and the total fat pad (TFP) were collected for analysis. Results: Carnitine supplementation, tended to decrease body weight, TFP, TAG content and serum FFA, and significantly decreased the TL content, serum leptin, TAG (P<0.0005). Carnitine feeding resulted in a significant elevation of serum carnitine, β-HBA and urinary carnitine (P<0.0005), compared to sedentary control rats. These values became more pronounced on choline addition to the diet except for serum and urinary carnitine that reversed (i.e. decreased) by choline addition. Exercise intervention resulted in a significant decrease in body weight, TFP, TL content and serum leptin, TAG and FFA. These values were more pronounced in both supplements with exercise, specially serum carnitine. However, exercise caused reduction of urinary carnitine in non-supplemented and carnitine supplemented groups and this was reversed by choline and exercise. Conclusion: Our study demonstrated that the beneficial effects of carnitine supplements is promoted by choline with or without mild exercise to reduce body weight, body fat, serum leptin and promote fat loss by increasing lipolysis as indicated by increased serum β-HBA. These results may or may not be applicable to humans, so further research is recommended to determine whether similar effects would result in humans or not.

Dietary carnitine intake and carnitine status in endurance‐trained males

AbstractBackground: Carnitine is an integral component of fatty acid transfer into the mitochondria, and also buffers excess intramitochondrial acyl‐CoA. It has previously been suggested that athletes may be at risk of low carnitine status and could therefore benefit from carnitine supplementation.Objective: To report the habitual dietary carnitine intakes of endurance‐trained adult males, and to determine whether they are at risk of carnitine insufficiency by measuring plasma and urinary carnitine concentrations.Methods: Fourteen non‐vegetarian endurance‐trained males completed a seven‐day weighed food record and exercise logs to determine habitual dietary carnitine intake. Resting venous blood samples and 24‐hour urine collections were used to determine plasma carnitine concentration and urinary carnitine excretion.Results: The mean dietary carnitine intake was 64 (range 21–110) mg/day. Mean ± SD resting plasma total carnitine was 44 ± 7 µmol/L and acyl : free carnitine ratio was 0.28 ± 0.11, which were within normal ranges. Urinary carnitine excretion was 437 ± 236 µmol/day. There was no correlation between dietary carnitine intake or dietary macro‐ and micronutrients and plasma carnitine or urinary carnitine excretion.Conclusion: The results of the present study indicate there is no evidence that endurance‐trained males consuming a mixed diet are at risk of carnitine insufficiency.