L-carnitine and metabolic rate -
q The apex end of the bag was fitted with an airtight 3-way stopcock that permitted syringe collection of expired gas. Breath samples were collected only after the bag was filled and emptied a minimum of 3 times.
Collected gas samples were immediately injected into mL evacuated gas collection vials r and stored at room temperature until batched analyses. Isotope measurements were performed by means of source isotope-ratio mass spectrometry.
s Plasma palmitate concentrations were measured in accordance with a standard method for FFA. in which Eb is the degree of enrichment of breath CO 2 , Ep is the degree of enrichment of palmitate in plasma, and k is correction factor for retention of bicarbonate in blood estimated as 0.
Nitrogen balance —Degree of nitrogen balance was determined from the amount of nitrogen consumed in weighed food on a daily basis and the amount of nitrogen eliminated in urine and feces.
Stoichiometric substrate oxidation rate —Estimates of substrate oxidation rates were made on the basis of indirect calorimetry gaseous exchange estimates and calculations according to the method of Frayn. in which 1 g of urinary nitrogen was assumed to reflect 6. Stoichiometric substrate calculations were completed for days 0, 42, and Statistical analysis —Summary statistics are reported as mean ± SD for normally distributed data or as median range for nonnormally distributed data.
Box-and-whisker plots, histograms, and the Kolmogorov-Smirnov test were used to evaluate the data for a Gaussian distribution, with the aid of statistical software. t For intergroup comparisons, ANOVA for repeated measures or ANCOVA was used when data were normally distributed and Kruskal-Wallis ANOVA was used for other data fold increase in palmitate flux rate among diet groups.
Differences in energy expenditure among groups were evaluated via ANCOVA, with DEE or REE as the dependent variable, diet and LBM as independent variables, and body weight as a covariate. Significant interactions of the independent variables with REE necessitated data transformation as described elsewhere.
Differences in RQ were evaluated relative to baseline values within groups and relative to control group values for all cats that received carnitine on a per group and combined collective basis because of a concern that the small group size would limit the power to detect differences that truly existed.
Two × 2 tables were used to evaluate differences between diet groups in cats achieving an IBW within the study period. Box-and-whisker plots were used to display range, median, and mean values for nonparametric data. Animals —With the exception of 1 cat in the control group that was removed from the study because of intractability, all cats completed the study.
Diet groups were equivalent with respect to sex distributions, body weight, estimated IBW, and BCS before the diet trial began Table 1. Mean age in the groups were equivalent data not shown. Hematologic, serum biochemical, and urine analyses performed throughout the study did not reveal any abnormalities or signs that hepatic lipidosis had developed data not shown.
For REE and RQ, 5 cats were censored from calculations involving day 84 data because those cats achieved targeted body weight between days 42 and 84 and were subsequently provided food allowances to maintain stable body weight. Energy ingestion during unrestricted and restricted feeding periods —Results of analysis of the weight reduction diets were summarized Table 2.
No significant differences in daily food intake mass or energy were detected among groups during any phase of the study Table 3. See Table 2 for description of weight reduction diets. As expected, rapid rebound weight gain occurred with unrestricted feeding of the energy-dense diet days 85 to , with cats gaining a mean of 0.
Some cats gained as much as 1. Percentage cumulative weight gain ranged from 6. Weight gain with ad libitum feeding of the energy-dense diet on days 85 to is represented as cumulative increase in body weight kg and as percentage increase of body weight on day Mean daily food consumption was 57 ± Mean daily energy ingestion was ± Daily energy expenditure was determined with doubly labeled water.
Resting energy expenditure was measured by means of indirect calorimetry. The greatest weight loss in these cats occurred during days 43 to Five cats fed carnitine-supplemented diets achieved their target IBW before day 84 1 cat in the CN group, 1 in the CN group, and 3 in the CN group and had energy intake adjusted to maintain body weight thereafter.
Adherence to study protocol resulted in censoring of indirect calorimetry data from these cats on day 84 because they were not continuing to undergo weight loss but were instead fed to maintain optimal body condition. Indirect calorimetry —No significant differences were detected among groups with respect to REE values at baseline Figure 1.
Citation: American Journal of Veterinary Research 73, 7; That observation corresponded to findings during unrestricted access to the energy-dense diet fed during baseline and days and , compared with the restricted feeding of weight reduction diets days 1 to 84 , despite the higher fat content of the energy-dense diet.
Cats that received no carnitine had mean RQs at baseline, day , and day of 0. Considering that baseline RQ reflected ingestion of a comparatively high-fat, energy-dense diet FQ, 0. The finding that the RQ had significantly decreased in cats that consumed carnitine-supplemented diets was further substantiated by the RQ increase in each carnitine-supplemented group upon restoration of unrestricted feeding of the higher fat energy-dense diet which was not carnitine supplemented from days through Palmitate oxidation —No significant differences were evident among diet groups in rates of palmitate flux or oxidation or estimated fatty acid appearance oxidation at baseline Figures 3 and 4.
Rates of palmitate flux and estimated FFA oxidation were significantly higher on day 42 than at baseline in the unsupplemented, CN, and CN groups, as would be expected with weight loss.
The onerous nature of the palmitate perfusion procedure precluded evaluations on more days than baseline and day Stoichiometric calculation of substrate oxidation —Stoichiometric calculation of substrate oxidation was limited to days in which LBM had been determined.
With the exception of the CN group, there were no differences in estimated substrate oxidation between carnitine-supplemented and unsupplemented diet groups at baseline Figure 6. Median estimated fat oxidation rate at baseline in the CN group was However, the percentage increase in estimated fat oxidation in the control and CN groups were similar with median increases of This finding suggested that the group fed the unsupplemented diet maintained a higher rate of carbohydrate use, compared with the carnitine-supplemented groups.
The present study involved several techniques to determine whether dietary l -carnitine supplementation during weight reduction alters fatty acid oxidation rate, REE, or LBM in overweight cats.
Stable isotope methods estimating DEE and LBM were combined with indirect calorimetry and stable isotope labeled palmitate infusion to investigate metabolic responses.
Few studies 30,31 have been conducted to investigate the influence of l -carnitine supplementation on fatty acid oxidation, and none have simultaneously measured energy expenditure and LBM or involved use of customized palmitate infusions as was done in the present study.
Baseline measurements in the absence of supplemental l -carnitine were conducted before weight loss was initiated in the present study, and all variables for cats that received supplemental l -carnitine were compared over the study period with baseline measurements and measurements from a control group that received no supplemental carnitine.
Also, because metabolic findings in the present study were compared with those obtained during feeding of a high-fat, energy-dense diet at baseline, it is probable that more extreme changes in fat oxidation and RQ would occur in similar studies of cats with stable body weights at baseline that receive a lower-fat, less energy-dense diet.
Unrestricted feeding of the weight reduction diets achieved a weekly rate of weight loss ranging from 0. Initial diet acceptance with the abrupt dietary change was variable among cats, with some hesitant to eat the new diet during the first 2 to 7 days cats ate smaller amounts, but none failed to eat altogether.
In most cats, quantitative consumption progressively increased over the 4 weeks of unrestricted feeding. In a few cats, there was little or no change in the amount of food ingested during the first week of diet introduction. The first weeks after diet introduction are believed to represent the period of highest risk for development of hepatic lipidosis in pet cats that are reluctant to consume the newly introduced food.
To minimize this risk, gradual introduction of the new food by mixing it with the current food is generally recommended.
Although the diet change was abruptly introduced in the present study, there was no evidence of an adverse effect on hematologic or biochemical variables secondary to reduced energy intake. Responses of the study cats to unrestricted feeding of the weight reduction diet suggested that this strategy may be used for initiating, sustaining, or transitioning cats with poor intake control glutonous feeding behavior to a more rigorous weight control program.
As expected, unrestricted diet consumption still exceeded the daily energy allowances calculated to achieve weight reduction during the period the diet was fed. Mean weekly weight loss exceeded 1.
There were no significant differences in rate of weight loss or total achieved weight loss between carnitine-supplemented and unsupplemented diet groups during feeding of the weight reduction diet.
However, there were no significant differences between cats that did or did not receive the carnitine supplement. Therefore, collective findings regarding absolute weight reduction do not suggest an obvious benefit of dietary carnitine supplementation.
The inconsistent response to dietary carnitine supplementation and the lack of a significant influence on weight loss and body condition change increased LBM , compared with findings in the control group, were at odds with the indirect calorimetry findings of a carnitine-enhanced rate of fatty acid oxidation.
These disparate results might have been a result of limited statistical power too few cats , individual variation among cats, or a differing influence of carnitine-supplements given in amounts exceeding physiologic requirements.
Although interpretation of change in gross body weight is complicated by the higher density and weight of muscle than in fat, change in LBM at endpoint of the weight reduction protocol was not different between the carnitine-supplemented and unsupplemented diet groups.
Because LBM was determined by isotope dilution, it was only quantified on 3 days baseline and days 42 and 84 so that LBM could be used for REE normalization. A significant decrease in REE per LBM was observed only in cats fed the unsupplemented diet on days 42 and Whether that decrease reflected an influence of carnitine supplementation or individual variation remains to be substantiated through additional studies.
An influence of adaptive thermogenesis in lowering REE during and after weight loss is a possible explanation, but this phenomenon remains controversial.
Still other investigators have reported no detectable change in REE or DEE accompanying or after weight loss. Carnitine ingestion in the present study might have protected against adaptive thermogenesis as a means of sustaining metabolic rate.
Consequently, the power to identify significant change in DEE among the diet groups, if it indeed existed, was low. Although metabolic effects of carnitine ingestion were variable and mild, cats fed the l -carnitine-supplemented diets sustained their REE per LBM kg , suggesting protection against adaptive thermogenesis during weight loss.
This interpretation is supported by the finding of a significant reduction in RQ on day 42 in cats fed carnitine-supplemented diets and the consistently observed lower RQ in the combined analysis of all such cats relative to cats fed the unsupplemented diet throughout the restricted feeding period.
Furthermore, upon reinstitution of unrestricted feeding of the energy-dense diet days 85 to , the REE increased in the control group, suggesting the observed difference from the other groups during the restricted-feeding phase of the study might have indeed been attributable to carnitine.
The RQ significantly increased in all cats during reinstitution of unrestricted feeding of the energy-dense diet, despite the lower FQ relative to the weight reduction diet.
This change in RQ consistent with a lower rate of fatty acid oxidation might simply have reflected cessation of weight loss or, alternatively, withdrawal of carnitine supplements.
Food restriction resulted in a significant decrease in urinary nitrogen elimination, as expected, and there was no apparent influence of l -carnitine supplementation on nitrogen conservation.
However, protein turnover rate was not specifically investigated. Weight reduction was associated with an increased percentage of palmitate oxidation and fatty acid flux rate estimated by 1- 13 C-palmitate infusions in each group, although values differed widely among individual cats.
These findings also suggested that the diets supplemented with greater amounts of carnitine augment fatty acid oxidation. Several measured variables reflecting fatty acid oxidation rate during weight loss in overweight cats were investigated in the present study.
Initial estimated rates of FFA turnover in cats at baseline were approximately 2- to 3-fold as great as those in humans 7. Although FFA appearance rates were in agreement with values previously reported for cats, 42,43 baseline values reflected consumption of the high-fat energy-dense diet as well as 12 hours of food restriction.
Indirect calorimetry findings suggested that carnitine might protect against a decrease in metabolic rate in the presence of weight reduction and enhance in vivo fatty acid oxidation in overweight cats undergoing rapid weight reduction.
However, the 13 C-palmitate infusion tests were unable to clearly demonstrate a similar carnitine effect, possibly because of the wide interindividual variability in palmitate oxidation. The final phase of the present study demonstrated the rapid rebound weight gain that may occur after substantial weight loss, upon reinstitution of unrestricted feeding of an energy-dense diet.
Findings during the last phase of study emulated the rapid rebound weight gain observed clinically in pet cats after successful weight reduction when owners fail to permanently modify feeding practices.
Results of the present study suggested that dietary supplementation with l -carnitine yields a metabolic effect on the basis of indirect calorimetry parameters and stoichiometric calculations that may be advantageous in overweight cats undergoing rapid weight reduction, complementing previous observations.
The mechanisms by which metabolic change might happen remain undetermined, but carnitine supplementation has been shown to augment the activity of feline hepatic carnitine-palmitoyltransferase kinase, which is a rate-limiting enzyme of acyl-carnitine transport at the mitochondrial membrane.
Because both fatty acid oxidation and egress of acetyl-carnitine from the liver might be enhanced by maximizing transporter activity, increasing acyl-carnitine transporter activity at the mitochondrial interface might have mechanistic relevance in anorexic overweight cats at risk for hepatic lipidosis.
This might explain clinical observations that dietary supplementation with l -carnitine improves the probability of survival time in cats severely affected with hepatic lipidosis when included as a component of nutritional support.
Cornell University Isotope Laboratory, Thermo Finnegan Delta Plus Isotope Ratio Mass Spectrometer, Brennan, Germany. Potassium palmitate-1 13C, catalog No. CLM, Cambridge Isotope Laboratories Inc, Andover, Mass.
Gelman Sciences Supor Acrodisc 25, sterile single-use nonpyrogenic with psi pressure limitation, Pall Gelman, Sigma-Aldrich, St Louis, Mo.
Labco Exetainer SystemC and Gas Testing Vials 10 mL Gas ×, LabCo Ltd Brow Works, High Wycombe, Buckinghamshire, England. Mean nutrient contents of energy-dense fattening diets 1 and 2 fed without restriction before and after the study and the weight reduction diet.
Sign in Sign up. Advanced Search Help. American Journal of Veterinary Research. Publication Date: 01 Jul Export Figures. Figure 2— Mean ± SD RQ determined by indirect calorimetry in the cats in Figure 1.
Figure 3— Box-and-whisker plots of palmitate flux rate A and fold increase in palmitate flux rate B determined from 1- 13 C-palmitate steady-state infusion in the cats in Figure 1. Figure 4— Box-and-whisker plots of estimated FFA oxidation rate determined by 1- 13 C-palmitate steady-state infusion in the cats in Figure 1.
Figure 5— Box-and-whisker plots of daily nitrogen intake determined from food intake A and urinary nitrogen elimination by Kjeldahl analysis B for the cats in Figure 1. Figure 6— Box-and-whisker plots of stoichiometrically calculated rate of fat oxidation A and carbohydrate oxidation B in the cats in Figure 1.
View raw image Figure 2— Mean ± SD RQ determined by indirect calorimetry in the cats in Figure 1. View raw image Figure 3— Box-and-whisker plots of palmitate flux rate A and fold increase in palmitate flux rate B determined from 1- 13 C-palmitate steady-state infusion in the cats in Figure 1.
View raw image Figure 4— Box-and-whisker plots of estimated FFA oxidation rate determined by 1- 13 C-palmitate steady-state infusion in the cats in Figure 1. View raw image Figure 5— Box-and-whisker plots of daily nitrogen intake determined from food intake A and urinary nitrogen elimination by Kjeldahl analysis B for the cats in Figure 1.
View raw image Figure 6— Box-and-whisker plots of stoichiometrically calculated rate of fat oxidation A and carbohydrate oxidation B in the cats in Figure 1.
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Authors Tara Bidgood. Mark G. Short-term effect of therapeutic shoeing on severity of lameness in horses with chronic laminitis. Authors Danny Taylor. David M. Ilka P. Previous Article Next Article. Influence of dietary supplementation with l -carnitine on metabolic rate, fatty acid oxidation, body condition, and weight loss in overweight cats.
Sharon A. Center Sharon A. Center Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY Search for other papers by Sharon A. Center in Current site Google Scholar PubMed Close. Karen L. Warner Karen L. Warner Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY Search for other papers by Karen L.
Warner in Current site Google Scholar PubMed Close. John F. Randolph John F. Randolph Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY Search for other papers by John F.
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Online Publication Date: 01 Jul Full access. Sign In Reprints and Permissions Download PDF. Materials and Methods Animals —Thirty-two colony-housed adult cats age range, 3 to 7 years; 16 neutered males and 16 neutered females were used in the study. Results Animals —With the exception of 1 cat in the control group that was removed from the study because of intractability, all cats completed the study.
Group Body weight kg BCS IBW kg Unsupplemented 5. Discussion The present study involved several techniques to determine whether dietary l -carnitine supplementation during weight reduction alters fatty acid oxidation rate, REE, or LBM in overweight cats.
Mettler PC DeltaRange analytical balance, Mettler-Toledo Inc, Columbus, Ohio. Sierra Series mass flow controllers, Sierra Instruments Inc, Monterey, Calif. Drierite, anhydrous CaSO 4 , WA Hammond Drierite Co, Xenia, Ohio.
Ascarite II, Thomas Scientific, Swedesboro, NJ. Sable Systems CA-1 Carbon Dioxide Analyzer, Sable Systems, Las Vegas, Nev. Sable Systems FC-1 Oxygen Analyzer, Sable Systems, Las Vegas, Nev.
Datacam V, Analytical Software, Sable Systems, Las Vegas, Nev. Deuterium oxide, Sonicator Cell Disruptor, model No. W F, Heat Systems-Ultrasonics Inc, Plainview, NY.
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Composition of a diet used for weight reduction in cats. Ingredient Percentage of total content Chicken by-product meal The mTOR protein is one of the most important regulatory elements of protein synthesis 53 ; therefore, dietary supplementation with L-carnitine might have positive effects on protein synthesis in zebrafish.
In Atlantic salmon, dietary L-carnitine supplementation increased the amino acid concentration in plasma and the liver, especially the three branched-chain amino acids, including leucine, isoleucine, and valine, and increased the protein synthesis capacity, accompanied by the accumulation of protein in organs The studies in mammals and rainbow trout reported that leucine can effectively stimulate mTOR signalling 54 , Thus, we deduced that dietary L-carnitine supplementation can stimulate the expression of mTOR in fish by increasing the leucine concentration in the feeding state.
The specific mechanism of the protein sparing effect of L-carnitine is detailed in Fig. However, the present study also indicated that dietary L-carnitine supplementation significantly decreased the whole body protein content in the fasting state, and the gene expressions of ASNS and mTOR in the L-carnitine groups were also downregulated in the muscle in the fasting state.
This might be explained if L-carnitine accelerated the degradation of lipids and proteins in the fasting state, and inhibited the synthesis of lipids and proteins to larger degree compared with the control. Compared with the whole body glycogen content, which was increased in the L-carnitine supplementation group in the fasting state, the decreased lipid and protein content in L-carnitine supplementation group in the fasting state confirmed that fish prefer to utilize proteins and lipids rather than carbohydrates.
To illustrate the systemic regulation of nutritional metabolism by L-carnitine in zebrafish, the interaction of different metabolic pathways in the L-carnitine-fed fish is shown in Fig.
Meanwhile, dietary L-carnitine supplementation also inhibited glycolysis and enhanced gluconeogenesis to decrease glucose-derived energy production Fig.
In the fasting state, dietary L-carnitine supplementation had similar effects on lipid and glucose metabolism to the feeding state, but also increased protein degradation and reduced protein synthesis Fig.
Nevertheless, our results also indicated that the interaction effects between nutritional state and L-carnitine supplementation existed in many parameters, including nutrient compositions, biochemical activities and metabolism-related gene expressions.
This indicates that the regulatory mechanisms of L-carnitine in feeding or fasting states as shown in Fig. Furthermore, it is of note that the changes of gene mRNA expression do not directly reflect the enzyme activities or protein functions, therefore, the regulatory mechanisms of L-carnitine at the transcriptional level still need further functional validation.
The present study indicated that dietary L-carnitine supplementation could increase the concentrations of carnitine in the liver and muscle, and decrease the lipid content in both tissues, possibly through enhanced mitochondrial β-oxidation and reduced adipogenesis.
Dietary L-carnitine supplementation also increased the expression of mTOR in the liver, suggesting that it has positive roles in protein synthesis. However, dietary L-carnitine supplementation decreased glycolysis, because the increase in lipid-sourced ATP from L-carnitine supplementation might change the balance of energy homeostasis between lipids and carbohydrates.
This is the first study to explore the mechanism of the positive effect of L-carnitine on the nutritional metabolism at transcriptional and biochemical levels in fish.
All experiments were conducted strictly under the Guidance of the Care and Use of Laboratory Animals in China. This study was approved by the Committee on the Ethics of Animal Experiments of East China Normal University.
In order to avoid the metabolic disturbance of estrogen during the sexual maturation of female fish, only male zebrafish 0. After acclimation, six hundred zebrafish were randomly divided into 2 groups 3 tanks per group, fish per tank : control group and carnitine group Fig.
In the feeding trial, the carnitine was given by feeding fish with small wheat flour-dough particles containing L-carnitine carnitine group or not control group , before basic diet feeding. In the preparation of the L-carnitine-contained wheat flour-dough particles, L-carnitine was first dissolved in pure water, and the carnitine solution was mixed with given amount of wheat flour to make wet dough.
The formulations of the basal diet and wheat flour-dough particle are listed in Table 1. The basal diet and dough particles were pelleted to a proper size about 0. In the two feeding groups, the feeding strategy was the same as that in the previous 6 weeks.
In the two fasting groups, only dough particles were fed in the morning and the amount was decreased to 0. Because the physiological effects of dietary L-carnitine supplementation were normally observed after 6—8 weeks in other animals 24 , 57 , the duration of the present experiment was 7 weeks.
The experimental design was shown in Fig. The weight of the fish in each tank was recorded every one week, and the feeding amount was adjusted correspondingly. At the end of the experiment, the whole fish in each tank were anthesthetized on ice, and sampled to collect liver, muscle and visceral for molecular and biochemical indexes.
Hepatic, muscle and visceral triglyceride TG and whole fish glycogen were assessed by the commercial kit Jiancheng Biotech Co. The crude lipid of the whole fish body was tested by using methanol and chloroform as previously described Whole fish protein was measured by Kjeltec TM FOSS, Sweden.
Because of the little mass of zebrafish organs e. Total carnitine was defined as the concentration of carnitine in sample A, free carnitine was defined as the concentration of carnitine in sample B. An HPLC system Agilent Technologies, Palo Alto, USA and a triple-quadrupole mass spectrometer Agilent Technologies, Palo Alto, USA were used.
The data was acquired and analyzed using MassHunter software version 5. The total run time for sample analysis was 4. After the feeding trial, the whole liver and parts of muscle of 3 fish collected from each group were weighted and homogenized in the ice-cold 0.
The samples of homogenate were used for the immediate measurement of mitochondrial and peroxisomal [1- 14 C] palmitate β-oxidation. After 0. The pure radioactive ASP medium was collected using 0. Total RNA was isolated by using a Tri Pure Reagent Aidlab, Cnina. The quality and quantity of total RNA were tested by NANODROP Spectrophpto Thermo, USA.
cDNAs of tissues total RNA were synthesized using a PrimerScript TM RT reagent Kit with a gDNA Eraser Perfect Real Time Takara, Japan by S TM Thermal Cycler Bio-Rad, USA.
Elongation factor 1 alpha EF1α and β-actin were used as the reference genes The primers of EF1α and target genes Table 2 for Quentitative PCR qPCR were designed to overlap intron.
The melting curves of amplified products were generated to ensure the specificity of assays at the end of each PCR. Each qPCR run performed in triplicate and negative controls no cDNA were conducted. Two-way ANOVA analysis was used to explore the possible interactions existing between nutritional states and L-carnitine supplementation in all parameters.
All analyses were conducted using the SPSS Statistics How to cite this article : Li, J. et al. Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio. Publisher's note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
A correction has been published and is appended to both the HTML and PDF versions of this paper. The error has been fixed in the paper. Scientific Reports 7: Article number: ; published online: 19 January ; updated: 23 March The original version of this Article contained an error in the spelling of the author Xuan Qin, which was incorrectly given as Xun Qin.
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in response to dietary chromium chloride supplementation. Trace Elem. Shiau, S. Carbohydrate utilization and digestibility by tilapia, Oreochromis niloticus × O.
aureus, are affected by chromic oxide inclusion in the diet. Leggatt, R. Growth hormone transgenesis influences carbohydrate, lipid and protein metabolism capacity for energy production in coho salmon Oncorhynchus kisutch. Panserat, S. Glucose metabolic gene expression in growth hormone transgenic coho salmon.
Polakof, S. Regulation of de novo hepatic lipogenesis by insulin infusion in rainbow trout fed a high-carbohydrate diet. Borges, P. High dietary lipid level is associated with persistent hyperglycaemia and downregulation of muscle Akt-mTOR pathway in Senegalese sole Solea senegalensis.
High dietary lipids induce liver glucosephosphatase expression in rainbow trout Oncorhynchus mykiss. Figueiredosilva, A. High levels of dietary fat impair glucose homeostasis in rainbow trout. He, A. Physiological Reports 3 , e PubMed PubMed Central Google Scholar.
Ji, H. Atlantic salmon Salmo salar fed L-carnitine exhibit altered intermediary metabolism and reduced tissue lipid, but no change in growth rate. Wang, X. The mTOR pathway in the control of protein synthesis. Physiology 21 , — Kimball, S.
Signaling pathways and molecular mechanisms through which branched-chain amino acids mediate translational control of protein synthesis. Lansard, M. L-leucine, L-methionine, and L-lysine are involved in the regulation of intermediary metabolism-related gene expression in rainbow trout hepatocytes.
Kita, K. Dietary L-carnitine increases plasma insulin-like growth factor-I concentration in chicks fed a diet with adequate dietary protein level. Kaya, I. Lambert, P. Seasonal variations in biochemical composition during the reproductive cycle of the intertidal gastropod Thais lamellosa Gmelin Gastropoda, Prosobranchia.
Veerkamp, J. Incomplete palmitate oxidation in cell-free systems of rat and human muscles. Biochemical hepatic alterations and body lipid composition in the herbivorous grass carp Ctenopharyngodon idella fed high-fat diets. Tang, R. Acta Biochimica et Biophysica Sinica 39 , — Download references.
This research was funded by National Basic Research Program of China program CB , National Natural Science Fund and , and Program for New Century Excellent Talents in University. Laboratory of Aquaculture Nutrition and Environmental Health LANEH , School of Life Sciences, East China Normal University, Shanghai, China.
Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China. You can also search for this author in PubMed Google Scholar. and J.
designed the research. and L. conducted the research. and M. analyzed data. and X. contributed to the final writing of the paper. and Z. wrote the manuscript. All authors have read and approved the final manuscript. Correspondence to Xin Wang or Zhen-Yu Du.
This work is licensed under a Creative Commons Attribution 4. Reprints and permissions. Li, JM.
L-carnitine and metabolic rate days 1 Fat burn accountability 84, L-catnitine of the same weight reduction diet was L-csrnitine. From days 84 tocats were fed an unrestricted amount of an energy-dense L-carnitinne. Mean ± SD L-carnitine and metabolic rate determined by indirect calorimetry in the cats in Figure 1. A—On day 84, 5 cats were censored because they had already achieved an IBW were no longer on energy restriction. B—Results for all cats fed carnitine-supplemented diets were combined. See Figure 1 for remainder of key. Box-and-whisker plots of palmitate flux rate A and fold increase in palmitate flux rate B determined from 1- 13 C-palmitate steady-state infusion in the cats in Figure 1.L-carnittine you for visiting nature. You are using a browser version anr limited support for CSS. L-carhitine obtain the best experience, we L-carniyine you use a Cognitive function boosting strategies up to date browser or turn off compatibility mode in Metabolism booster for men Explorer.
In the meantime, to ensure continued support, we are displaying the site without styles and Waist measurement and obesity prevention. A Corrigendum to this adn was published on 23 March Excess fat L-caritine has been ketabolic widely in farmed fish; therefore, efficient lipid-lowering factors have obtained high attention in the current fish nutrition tate.
Dietary L-carnitine can metaboli fatty acid β-oxidation Mindfulness in sports nutrition mammals, but has produced contradictory L-carnittine in metabo,ic fish species.
To date, the mechanisms Fermented foods for overall wellbeing metabolic regulation of L-carnitine in fish have not been fully determined. The present study used zebrafish to investigate the L-carbitine regulation L-crnitine nutrient metabolism mrtabolic dietary L-carnitine supplementation.
L-carnitine Examining nutrition myths decreased the L-carrnitine content in liver and muscle, accompanied by increased concentrations of Fueling for peak performance and free carnitine in tissues.
Meanwhile, L-carnitine enhanced mitochondrial L-carnnitine activities and the expression of carnitine palmitoyltransferase 1 mRNA significantly, whereas it depressed the mRNA expression of adipogenesis-related genes.
In metabloic, L-carnitine metagolic higher L-carnitine and metabolic rate deposition in the fasting state, and L-acrnitine and decreased the mRNA expressions metabolix gluconeogenesis-related and glycolysis-related genes, respectively.
Qnd also increased the metzbolic expression of mTOR in the L-carintine state. Taken together, Diuretic effect on digestive health L-carnitine supplementation decreased lipid deposition by increasing mitochondrial fatty acid β-oxidation, L-carnnitine is likely to promote protein LL-carnitine.
However, the L-carnitine-enhanced lipid catabolism would cause a decrease in L-carnotine utilization. Electrolyte Formula, L-carnitine has comprehensive effects on nutrient metabolism in fish.
Annd is L-carnigine important factor that regulates fatty metabilic FA and glucose metabollic to achieve balanced cellular energy metabolism 1. L-carnitine can be synthesized naturally from lysine L-carnktine methionine rqte microorganisms, Powerful antioxidant supplements and animals 2.
In L-carnitin and other mammals, L-carnitine deficiency rahe severe hyperlipidaemia and systemic metabolic syndrome L-caarnitine6.
Compared with other farmed animals, fish generally have a lower ability to use L-crnitine as energy sources; thus L-carnitinne higher levels of dietary proteins However, HFDs often lead to severe lipid accumulation in the liver and metabolci adipose tissues in farmed fish, and induce metabolic disturbances, an as Mettabolic liver and excess ,etabolic fat deposition 12 Therefore, regulatory L-canitine that could reduce lipid deposition L-cxrnitine fish, especially during Metaboic feeding, have attracted increased research attention.
The effective lipid-lowering effects of Non-pharmaceutical mood enhancer have led to Whole grain options for athletes hypothesis that L-carnitine in fish would have similar effects L-carniyine L-carnitine and metabolic rate in metsbolic and would rrate lipid utilization.
During recent decades, the potential nutritional functions of carnitine L-caarnitine been studied in many metabolc species; however, the results and conclusions differed. In Metaboolic sea bass 14 Meabolic, red sea bream L-carnitne and hybrid rage bass 16 metaboljc, carnitine promoted growth.
Lc-arnitine, this effect was not observed in channel catfish L-carnitine and metabolic rateL-carnitine and metabolic rate trout 18 and hybrid tilapia L-farnitine European sea Supporting healthy digestion 14Balanced diet plan tilapia 20Indian rafe carp rohu 21dietary carnitine supplementation could lower the L-carnitine and metabolic rate meyabolic in L-carnigine body and liver, and it improved the utilization of certain Pharmaceutical-grade ingredient consistency, such as eicosapentaenoic acid L-carnitiine and docosahexaenoic acid DHA in red L-carnitjne bream 15and African catfish However, carnitine supplementation anv no effects on lipid metabolism in Metabilic catfish 23hybrid Gestational diabetes and babys growth 19 and hybrid striped bass Indeed, carnitine even reduced lipid metabolism in L-carrnitine sea bream 15yellow catfish 24 abd rainbow trout L-carnitinne The contradictory and rzte results ketabolic carnitine supplementation L-carnitie fish have made the metsbolic utilization of Cellulite reduction foods in fish feed controversial.
This L-carnitihe largely restricted our understanding of the function metanolic carnitine in fish, and an explanation gate the conflicting rahe of metabolid application of gate in fish remains elusive. Anx, the ,etabolic of the effects of carnitine Antibacterial soap bar fish should be studied.
As a widespread model animal in research areas anf as Tart cherry juice for skin health, molecular genetics, tate and biomedicine 26 L-cqrnitine, 27zebrafish Danio rerio has been L-carnitine and metabolic rate in mechanistic studies of fish nutrition 28 In the amd study, zebrafish was used to L-carbitine the systemic regulation rahe lipid, protein Greek yogurt for athletes carbohydrate metabolism ane L-carnitine in fish in feeding and fasting states, respectively.
Moreover, the metabolic pathways associated with rat nutritional regulation by dietary L-carnitine Fuel Consumption Tracking System in zebrafish were determined.
To the best wnd our knowledge, this is the first study to demonstrate the metabolic mechanisms of nutritional Protein and weight management by dietary L-carnitine supplementation in fish.
Metbolic the experiment, the fish were Nutrient-rich fuel for the body good health and showed no growth metbolic compared with control fish L-carnitinne not shown.
To ans the effects of rahe carnitine supplementation on the endogenous carnitine concentrations, the carnitine Anti-cellulite diet plan in various fish L-carjitine were Body cleanse for toxins. In the liver and L-carnitine and metabolic rate, metabolkc in the Micronutrient fortification and fasting states, metbaolic free carnitine and total carnitine Arthritis alternative therapies in L-carnitine and metabolic rate carnitine supplementation group were significantly higher Antioxidant supplements for brain health in the control group Fig.
The mRNA levels of BBOX1the key enzyme for carnitine synthesis, were not significantly different in the liver and in fasting state muscle; however, in feeding state muscle, the BBOX1 mRNA level in the carnitine supplementation group was significantly higher than that in the control group Fig.
No L-carnittine difference was found in the whole fish lipid level in all groups Fig. Compared with the control group, the triglyceride TG content was significantly decreased in the carnitine supplementation group in the liver and muscle in both the feeding and fasting states; however, the TG content in the viscera was comparable in all groups Fig.
There were no interaction effects of the nutritional states and L-carnitine found in the whole fish lipid level and TG content in the different organs, except in the BBOX1 mRNA level Supplemental Table 1showing BBOX1 is simultaneously regulated by nutritional state and L-carnitine supplementation.
The above data indicated that dietary carnitine supplementation could increase the in vivo carnitine concentration and reduce the TG content in the liver and muscle. A Free carnitine; B Total canitine; C The relative mRNA abundance of carnitine synthesis gamma-butyrobetaine hydroxylase 1, BBOX1 ; D The crude lipid content of whole fish; E TG content of liver, muscle, viscera.
As shown in Fig. In the muscle, the mitochondrial and total β-oxidation capability in the feeding state were higher in the carnitine supplementation group than in the control, but showed no difference in the fasting state Fig.
There were no significant differences in the peroxisomal β-oxidation capability between the control and carnitine supplementation groups Fig. The significant interaction between the nutritional state and L-carnitine was only seen in the mitochondrial and total β-oxidation capability in muscle Supplemental Table 2.
The results showed that dietary L-carnitine supplementation targets the liver and muscle, and has a lipid-lowing effect that functions mainly through mitochondrial FA β-oxidation, but not via peroxisomal FA β-oxidation.
A The mitochondrial β-oxidation capability; B The peroxisomal β-oxidation capability; C The total β-oxidation capability. Figure 3 shows the effects of dietary L-carnitine on the mRNA expressions of genes related to lipid metabolism.
In the L-carnitine supplementation group, the mRNA level of the mitochondrial β-oxidation-related gene CPT1 was significantly increased Fig.
The mRNA level of LPL increased in the carnitine supplementation group in the liver in the feeding state but decreased in the muscle in the fasting state Fig. The other lipid metabolism-related genes, including HAD, ACOX3, CD36, ATGL and HSLremained unchanged in the livers and muscles of the two groups in the two states.
Interaction effects between the nutritional state and carnitine levels were observed in the mRNA levels of ACC, FASand DGAT2 in liver and muscle, and ATGL and LPL in liver Supplemental Table 3showing nutritional state and L-carnitine both regulated the lipid synthesis and lipolysis.
The results suggested that dietary L-carnitine could upregulate the mRNA expression of mitochondrial FA β-oxidation genes, and downregulate the mRNA expression of FA and TG synthesis genes in the liver and muscle.
The whole fish glycogen levels remained invariant in feeding states, but increased in fasting state Fig. However, the genes related to glucose metabolism were affected by dietary L-carnitine supplementation. The mRNA level of PFKa key glycolysis-related gene, was significantly decreased fasting state and increased feeding state in the muscle, but was comparable in the liver Fig.
The mRNA level of PKanother key glycolysis-related gene, was decreased in the muscle, and the decrease was significant in the feeding state Fig. The mRNA expressions of PECK1 and G6Pawhich are key gluconeogenesis-related genes, were significantly upregulated by dietary L-carnitine in the liver, but did not change in the muscle Fig.
The mRNA expressions of insulin sensitivity-related genes, including insulin, Ira and Irbwere mostly unaffected by dietary L-carnitine supplementation Fig. The interaction effects between the nutritional state and L-carnitine were only seen in the mRNA levels of PFK in muscle and PECK1 and Irb mRNA levels in liver Supplemental Table 4.
In general, the above data suggested that dietary L-carnitine supplementation tended to increase gluconeogenesis, but decreased glycolysis; therefore, L-carnitine supplementation lowered the utilization of glucose. The mRNA expressions of aminopeptidase N APN and oligopeptide transporter PEPT1which function in protein and amino acid digestion and absorption, and glutamate dehydrogenase 1a and 1b GDH1a, GDH1bwhich are essential in amino acid catabolism, were not affected significantly by dietary L-carnitine supplementation in the liver and muscle Fig.
The mRNA level of asparagine synthetase ASNSwhich plays roles in protein synthesis, was significantly decreased in the L-carnitine group in the fasting state, both the liver and muscle Fig.
Notably, in the L-carnitine supplementation group, the mRNA expression of mTORthe regulatory factor for protein synthesis, was significantly increased in the liver in the feeding state Fig. The interaction effects between the nutritional state and L-carnitine were observed in the whole fish protein content and the mRNA levels of PEPT1 in the muscle Supplemental Table 5.
These data suggested that dietary L-carnitine supplementation tended to increase protein degradation by inhibiting protein synthesis in the fasting state. However, the increased rare protein levels in whole fish and the increased mTOR expression in the liver of carnitine-fed zebrafish also showed that L-carnitine has positive effects on protein synthesis in the normal feeding period.
The expressions of three inflammation-related genes were measured to investigate the potential effects of dietary L-carnitine on inflammation. Among all groups, the mRNA expressions of IL-1β were comparable Fig. The mRNA level of TNF-αa strong inflammatory factor, was significantly decreased in the muscle of the L-carnitine supplementation group, in both the feeding and fasting states; however, no significant differences in the liver expression were found among the groups Fig.
The mRNA expression of TGF-β1a known anti-inflammatory factor, was significantly increased by dietary L-carnitine supplementation in the muscle in the feeding and fasting states; however, its expression in the liver was not changed by L-carnitine supplementation Fig.
The interaction effects between the nutritional state and L-carnitine were observed in the mRNA levels of IL-1β and TGF-β1 in liver and TNF-α in muscle Supplemental Table 6.
These data indicated that dietary L-carnitine is likely to rare roles in inflammation processes. As an essential factor in mitochondrial FA β-oxidation, L-carnitine has been used to alleviate fat accumulation-related metabolic syndromes in humans and other mammals for decades 89 However, the effects of dietary carnitine supplementation in different fish species are contradictory 31but few previous studies performed comprehensive assays of lipid metabolism.
In the present study, although growth promotion was not observed in zebrafish, dietary L-carnitine supplementation decreased the TG content in liver and muscle significantly, but did not affect the level in the viscera. Considering that liver and muscle, but not adipose tissue, are the main tissues for FA β-oxidation, the liver and muscle should be the main target tissues of dietary L-carnitine supplementation in fish.
Indeed, the carnitine concentration in the liver and muscle of the experimental zebrafish increased with dietary L-carnitine supplementation. By measuring the β-oxidation of [1- 14 C] palmitate in the mitochondria or peroxisome of the liver or muscle, the present study first indicated that dietary L-carnitine supplementation mainly increased mitochondrial FA β-oxidation activity, but not peroxisomal activity, at least in zebrafish.
This was also confirmed by the high expression of CPT1 mRNA in the liver and muscle of the L-carnitine-fed zebrafish, and the comparable mRNA expressions of ACO in both tissues between the groups. The present study also indicated that dietary L-carnitine supplementation downregulated significantly the expression of adipogenesis-related genes, such as ACC, FAS and DGAT.
Therefore, the lipid-lowing effects of dietary L-carnitine supplementation in the present study are likely to be caused by increased mitochondrial FA β-oxidation activity and decreased lipid synthesis, which was in consistent with some mammalian studies 32 Mammalian and human studies showed that dyslipidaemia is accompanied frequently by inflammation 34 ; however, the L-carnitine-induced upregulation of CPT1 has been shown to prevent inflammation by decreasing inflammatory cytokines, such as TNF-α, in serum and the liver 30 Similarly, in the present study, L-carnitine supplementation significantly increased the expression of CPT1, accompanied by decreasing and increasing the mRNA expression of TNF-α and the anti-inflammatory factor TGF-β1, respectively, in zebrafish muscle.
This is the first report of this anti-inflammatory effect of L-carnitine in fish. Lipid accumulation-related metabolic dysfunctions have been observed widely in aquatic animals; therefore, the anti-inflammatory effects of L-carnitine in fish require further study. Compared with mammals, fish have lower abilities to use carbohydrates as energy sources, thus fish cannot use glucose to produce energy efficiently A number of studies have indicated that, as compared with mammals, the responses of the activities of many glucose metabolism-related key enzymes, such as GK, PFK and PK, are not sensitive to the increased dietary carbohydrate content in fish 36 In many fish species, high dietary carbohydrate induced lower growth, excess lipid deposition, and decreased stress resistance 3839 chromium 4344or even developing gene-modified fish species 45 However, in many fish species, these efforts are not ideal, and the regulatory mechanisms of carbohydrate metabolism are still poorly understood in fish.
Recently, the interaction between lipid metabolism and carbohydrate metabolism has been observed in fish 47 The phenomena that high-fat diet impairs glucose homeostasis has been reported in rainbow trout 49 Our recent work further illustrated that glycolysis-related genes are upregulated or downregulated during low-fat diet or high-fat diet feeding, respectively In the present study, dietary L-carnitine supplementation improved lipid catabolism significantly, but increased the whole body glycogen deposition in the fasting state, indicating that glucose degradation was inhibited.
: L-carnitine and metabolic rate| The Science behind Metabolism and L-Carnitine for Effective Fat Loss | Coleman A, Freeman P, Steel S, Shennan A. Conclusions Lasting for several years opinion that LC supplementation does not change metabolism, especially exercise metabolism, is based mostly on short-term supplementation protocols. Aquaculture , 3—21 Individual orts were measured and recorded daily. L-carnitine is an important factor that regulates fatty acid FA and glucose metabolism to achieve balanced cellular energy metabolism 1. Trained vs untrained evaluator assessment of body condition score as a predictor of percent body fat in adult cats. |
| L-Carnitine - Metabolic Functions and Meaning in Humans Life | Bentham Science | Close Print this page. Export Options ×. Export File: RIS for EndNote, Reference Manager, ProCite. Content: Citation Only. Citation and Abstract. About this article ×. Cite this article as: Pekala Jolanta, Patkowska-Sokola Bozena, Bodkowski Robert, Jamroz Dorota, Nowakowski Piotr, Lochynski Stanislaw and Librowski Tadeusz, L-Carnitine - Metabolic Functions and Meaning in Humans Life, Current Drug Metabolism ; 12 7. Close About this journal. Related Journals Current Drug Delivery. Drug Delivery Letters. Recent Advances in Drug Delivery and Formulation. Drug Metabolism and Bioanalysis Letters. View More. Mixed Polymeric Micelles for Osteosarcoma Therapy: Development and Characterization. A Comprehensive Text Book on Self-emulsifying Drug Delivery Systems. Nanomaterials: Evolution and Advancement Towards Therapeutic Drug Delivery Part I. Article Metrics. Journal Information. For Authors. Author Guidelines Graphical Abstracts Fabricating and Stating False Information Research Misconduct Post Publication Discussions and Corrections Publishing Ethics and Rectitude Increase Visibility of Your Article Archiving Policies Peer Review Workflow Order Your Article Before Print Promote Your Article Manuscript Transfer Facility Editorial Policies Allegations from Whistleblowers Announcements Forthcoming Thematic Issues. For Editors. Guest Editor Guidelines Editorial Management Fabricating and Stating False Information Publishing Ethics and Rectitude Ethical Guidelines for New Editors Peer Review Workflow. For Reviewers. Reviewer Guidelines Peer Review Workflow Fabricating and Stating False Information Publishing Ethics and Rectitude. Explore Articles. Abstract Ahead of Print 0 Article s in Press 1 Free Online Copy Most Cited Articles Most Accessed Articles Editor's Choice Thematic Issues. Open Access. Open Access Articles. This decrease in metabolic rate can lead to weight gain and difficulties in shedding excess fat. Furthermore, an unhealthy lifestyle characterized by poor dietary choices, sedentary behavior, and inadequate exercise can further contribute to a sluggish metabolism. L-Carnitine, a naturally occurring compound in the body, plays a pivotal role in the transportation of fatty acids into the mitochondria—the powerhouses of our cells—where they are burned for energy. This process is crucial for efficient fat metabolism. Acting as a carrier molecule, L-Carnitine facilitates the transport of long-chain fatty acids across mitochondrial membranes, enabling effective metabolism. Numerous studies have investigated the potential benefits of L-Carnitine in promoting fat loss and optimizing metabolic efficiency. Research suggests that L-Carnitine supplementation may enhance fat oxidation, leading to increased utilization of stored fat as an energy source during exercise. This effect can be particularly advantageous for individuals aiming to lose weight or enhance athletic performance. demonstrated that L-Carnitine supplementation resulted in a significant increase in fat oxidation during exercise, providing evidence of its role in supporting efficient fat metabolism. L-Carnitine's benefits extend beyond fat metabolism. Studies have indicated that L-Carnitine supplementation can enhance exercise performance by reducing muscle damage, promoting faster recovery, and optimizing energy utilization. By increasing the availability of fatty acids for fuel, L-Carnitine may help preserve muscle glycogen, thereby extending endurance and delaying fatigue during physical activity. observed that L-Carnitine supplementation improved exercise performance by delaying fatigue and enhancing recovery, underscoring its potential as an ergogenic aid. A comprehensive understanding of metabolism is essential for those striving to achieve sustainable weight loss and overall well-being. Aging and an unhealthy lifestyle can impede metabolism, making weight management more challenging. However, L-Carnitine supplementation has demonstrated promising results in enhancing fat-burning efficiency and exercise performance. Sova Health's Metabolic Fuel presents a science-backed solution, utilizing the power of L-Carnitine to unlock optimal fat metabolism and help individuals attain their weight loss goals. Powered by Shopify. Your cart. Free shipping for any orders above Rs. Continue shopping. all products shipped within 24 hours. Shop By Category. Gut Health Programs. Expert Consultation. Gut Microbiome Test. Expert Recommended Kits. View All. Shop By Concern. Weight Loss. |
| ORIGINAL RESEARCH article | Doxorubicin: Treatment with L-carnitine may protect heart cells against the toxic side effects of doxorubicin, a chemotherapy medication used to treat cancer, without making the medication any less effective. Always talk to your oncologist before using complementary or alternative CAM therapies with chemotherapy. Isotretinoin Accutane : Accutane, a strong medication used for severe acne, can cause liver problems, as measured by a blood test, as well as high cholesterol, and muscle pain and weakness. These symptoms are like those seen with carnitine deficiency. Researchers in Greece showed that a large group of people who had side effects from Accutane got better when taking L-carnitine compared to those who took a placebo. Thyroid hormone: Carnitine may stop thyroid hormone from getting into cells, and theoretically may make thyroid hormone replacement less effective. If you take thyroid replacement hormone, talk to your provider before taking carnitine. Valproic acid Depakote : The antiseizure medication valproic acid may lower blood levels of carnitine. Taking L-carnitine supplements may prevent any deficiency and may also reduce the side effects of valproic acid. However, taking carnitine may increase the risk of seizures in people with a history of seizures. Blood Thinning Medications: Carnitine may increase the risk of bleeding in people taking blood thinning medicaitons. Benvenga S, Ruggieri RM, Russo A, Lapa D, Campenni A, Trimarchi F. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind placebo-controlled clinical trial. J Clin Endocrinol Metab. Berni A, Meschini R, Filippi S, Palitti F, De Amicis A, Chessa L. L-carnitine enhances resistance to oxidative stress by reducing DNA damage in Ataxia telangiectasia cells. Mutat Res. Biagiotti G, Cavallini G. Acetyl-L-carnitine vs tamoxifen in the oral therapy of Peyronie's disease: a preliminary report. BJU Int. Carrero JJ, Grimble RF. Does nutrition have a role in peripheral vascular disease? Br J Nutr. Cavallini G, Modenini F, Vitali G, et al. Acetyl-L-carnitine plus propionyl-L-carnitine improve efficacy of sildenafil in treatment of erectile dysfunction after bilateral nerve-sparing radical retropubic prostatectomy. Cruciani RA, Dvorkin E, Homel P, Malamud S, Culliney B, Lapin J, Portenoy RK, Esteban-Cruciani N. J Pain Symptom Manage. Custer J, Rau R. Johns Hopkins: The Harriet Lane Handbook. Philadelphia, PA; Elsevier Mosby; Dyck DJ. Dietary fat intake, supplements, and weight loss. Can J Appl Physiol. Fugh-Berman A. Herbs and dietary supplements in the prevention and treatment of cardiovascular disease. Prev Cardiology. Head KA. Peripheral neuropathy: pathogenic mechanisms and alternative therapies. Altern Med Rev. Hiatt WR, Regensteiner JG, Creager MA, Hirsch AT, Cooke JP, Olin JW, et al. Propionyl-L-carnitine improves exercise performance and functional status in patients with claudication. Am J Med. Lynch KE, Feldman HI, Berlin JA, Flory J, Rowan CG, Brunelli SM. Effects of L-carnitine on dialysis-related hypotension and muscle cramps: a meta-analysis. Am J Kidney Dis. Malaguarnera M, Cammalleri L, Gargante MP, Vacante M, Colonna V, Motta M. L-carnitine treatment reduces severity of physical and mental fatigue and increases cognitive functions in centurians: a randomized and controlled clinical trial. Am J Clin Nutr. Miyagawa T, Kawamura H, Obuchi M, et al. Effects of oral L-carnitine administration in narcolepsy patients: a randomized, double-blind, cross-over and placebo-controlled trial. PLoS One. In cells, it helps transport fatty acids into the mitochondria, where they can be burned for energy. L-carnitine may help increase mitochondrial function, which plays a key role in disease and healthy aging 1 , 10 , L-carnitine is an amino acid derivative that transports fatty acids into your cells to be processed for energy. It is made by your body and also available as a supplement. One review of 37 studies found that L-carnitine supplementation significantly reduced body weight, body mass index BMI , and fat mass. However, it had no effect on belly fat or body fat percentage Another analysis of nine studies — mostly in individuals with obesity or older adults — found that people lost an average of 2. Furthermore, while it may aid in weight loss for some people, you may wish to consult with a dietician to develop a thorough diet and exercise regimen first. Some studies suggest that L-carnitine could help promote weight loss and fat loss. However, more studies are needed. Some research suggests that the acetyl form, acetyl-L-carnitine ALCAR , may help prevent age-related mental decline and improve markers of learning In fact, according to one study, taking 1, milligrams mg of ALCAR daily for 28 weeks significantly improved brain function in people with dementia For instance, a review of two studies showed that taking L-carnitine for 3 days had no effect on markers of brain function — including reaction time, vigilance, immediate memory, and delayed recall — in young adults without cognitive impairment L-carnitine — specifically acetyl-L-carnitine — may have beneficial effects on brain function. Still, more research is needed. For example, one review of 10 studies found that L-carnitine significantly reduced diastolic blood pressure, especially in people with overweight and obesity Another analysis of 17 studies showed that L-carnitine could improve heart function and decrease symptoms in people with congestive heart failure Additionally, a review showed that L-carnitine could reduce total and LDL bad cholesterol while increasing HDL good cholesterol in people at risk for heart disease The evidence is mixed when it comes to the effects of L-carnitine on sports performance, but it may offer some benefits. This differs from supplements like caffeine or creatine , which can directly enhance sports performance 22 , A recent review of 41 studies concluded that L-carnitine supplementation could reduce fasting blood sugar and hemoglobin A1c a marker of long-term blood sugar levels while also improving insulin sensitivity in people with diabetes, overweight, or obesity According to the authors of the review, L-carnitine is believed to work by altering insulin receptors and changing the expression of specific genes that regulate sugar metabolism It may also help improve the function of beta cells, which are cells in the pancreas that are responsible for producing insulin In one review of 12 studies, acetyl-L-carnitine significantly reduced symptoms of depression compared with placebo Interestingly, several of the studies included in this review also found that acetyl-L-carnitine was as effective as antidepressant medications but caused fewer adverse effects Research suggests that L-carnitine may aid exercise performance and treat health conditions like heart disease, depression, and type 2 diabetes. For most people, taking 2 grams g or less per day is relatively safe and free from any serious side effects Some research has also used doses of up to 4, mg per day However, there were some mild side effects, including heartburn and indigestion However, L-carnitine supplements may raise your blood levels of trimethylamine-N-oxide TMAO over time. High levels of TMAO are linked to an increased risk of atherosclerosis — a disease that clogs your arteries Doses of 2 g or less per day seem to be well tolerated and safe for most people. However, L-carnitine may increase levels of TMAO, which could be linked to an increased risk of plaque build-up. You can get small amounts of L-carnitine from your diet by eating meat and dairy products The best sources of L-carnitine are 35 :. As noted before, your body can also produce this substance naturally from the amino acids methionine and lysine if your stores are low. For these reasons, L-carnitine supplements are only necessary in special cases, such as disease treatment. The main dietary sources of L-carnitine are meat and some other animal products, such as milk. The interface exchange of acyl-CoA allows l -carnitine to facilitate the sharing of metabolic energy short-chain acyl-carnitine and acetyl-carnitine between intracellular organelles and tissues. Although supplemental l -carnitine has been shown to promote development of LBM during growth in piglets, its influence on body condition during weight loss remains controversial. However, no data exist to suggest dietary supplementation with l -carnitine results in a measurable in vivo change in substrate oxidation in overweight animals undergoing weight loss. The objective of the study reported here was to determine whether dietary supplementation with L-carnitine would facilitate weight loss in overweight cats fed a weight-reduction diet on an unrestricted or restricted basis, retention of LBM during weight loss, and preferential use of fat for energy expenditure substrate oxidation. Animals —Thirty-two colony-housed adult cats age range, 3 to 7 years; 16 neutered males and 16 neutered females were used in the study. Cats were allowed to become overweight through feeding of a mixture of 2 energy-dense dry diets provided without restriction for 6 consecutive months fattening diet; Appendix 1. Water was provided at all times throughout the experiment. Cats were individually housed for 19 hours daily and allowed recreational social interaction for the remaining 5 hours, except when indicated. During the initial fattening phase, cats were group housed with unrestricted exercise and social interactions during the day; unlimited quantities of food were available in their individual cages, where they were placed from 6 pm to 7 am. The housing and care provided to the cats were in compliance with the recommendations of the Institutional Animal Use and Care policies of Cornell University. Cats were returned to the fattening diet on days 85 through , with food provided without restriction. Investigators involved with experimental manipulations and cat handling remained unaware of which test diet each cat had received until the experiment had concluded and the data were analyzed. When a cat achieved IBW during the study, energy restriction was suspended and the cat was fed the same diet to maintain that body weight until day a The FQ of each diet was calculated as described elsewhere. Cat assessment —Body condition score was assigned at baseline day—28 and during the diet trial on a weekly basis by 2 investigators SAC and KLW experienced with this procedure. Other variables evaluated included daily food consumption determined from mass of food consumed and weekly body weight as determined with a calibrated digital scale b accurate to 0. REE analysis —Resting energy expenditure was determined with an open-flow indirect calorimetry system. Calorimetry measurements were performed in a softly lit room closed to pedestrian traffic with room temperature maintained between 18° and 20°C and temperature within the holding chamber maintained between 22° and 24°C. During calorimetry sessions, the activity of each cat was recorded to determine which measurements might reflect physical activity for their subsequent exclusion. Two to 3 weeks before data collection, cats were acclimated to the procedure. For the calorimetry sessions, cats were confined individually within a custom-built, clear, break-resistant chamber fitted with a sliding door perforated for ventilation with atmospheric air. Vacuum-driven cross-cage gas flow allowed collection of expiratory gas as it exited the holding chamber. Two cages with different dimensions Plastic-encased closed-cell extruded polystyrene foam inserts were used to reduce chamber dead space and tailor the cage fit to each cat. Cage dimensions and customization inserts were recorded to allow exact duplication of the calorimetry environment for serial data collection on different days. Each cage was configured to allow enough room for the cat to sit or recline comfortably with its head oriented toward the air intake vents in the sliding door. Initial gas flow was selected on the basis of the expected basal o 2 body weight [-kg 0. Because of the open-flow design, 14 the exact flow of gas across the holding chamber was verified by nitrogen dilution evaluations that were completed after each calorimetric session. Gas flow through a cage fitted with the closed-cell extruded polystyrene foam inserts and housing a replica cat was adequate to flush the system to ambient gas concentrations within 10 minutes after nitrogen dilution. A water absorbent d was positioned in line before the mass flow meters. Gas samples cage or ambient baseline gas first passed through a CO 2 sensor and then an O 2 analyzer linked in series. The CO 2 was removed from the system with a CO 2 absorbent e before gas delivery to the O 2 analyzer. The CO 2 concentrations were determined with an infrared-based analyzer, f and O 2 concentrations were measured with a disposable fuel cell. Fans were used to keep ambient gases well mixed, and the vacuum system providing cross-cage gas flow was evacuated through an environmental safety hood to the atmosphere. The system was calibrated to ambient air concentrations before, during, and after each recording session with a software controller. h After cats had acclimated to calorimetry cage confinement typically 20 minutes and steady-state CO 2 and O 2 concentrations were verified to exit the cage, expiratory gases were collected every 5 seconds for 45 minutes in 4 intervals. A customized data acquisition system h allowed automation of continuous chamber and periodic ambient environmental gas sample collection every 10 minutes during measurement sessions. Data from the mass flow meters, gas analyzers, and thermometer were continuously displayed and collected in real time during recording sessions via the automated data acquisition system. The o 2 for each analysis was calculated from the difference in O 2 concentration between airflow into and out of the chamber, with gas concentrations corrected to standard conditions for temperature and pressure. in which 3. The system registered a mean RQ of 0. Intra-assay REE repeatability was determined by collecting continuous measurements during three minute intervals on 1 day from 30 cats. LBM assessment —Measurements of LBM were completed in all cats on days 0, 42, and 84 by means of an established D 2 O protocol 18,19 within 5 days after open-flow indirect calorimetry assessments were performed. Cats were not manipulated for other testing during stable isotope tests. After 12 hours of food withholding, each cat was given D 2 O i 0. The exact dose of isotope delivered was determined gravimetrically by weighing the delivery syringe to the nearest 0. Blood samples were collected immediately before and 3 and 6 hours after isotope administration. Enrichment of D 2 O in serum was determined in triplicate by means of isotope ratio mass spectrometry j by estimating the degree of conversion of water to hydrogen in 2 μL of serum through the zinc-water reduction method. Cats were not manipulated for other testing during these evaluations. After 12 hours of food withholding, each cat received D 2 O i 0. The exact dose of isotope delivered was determined gravimetrically by weighing of the administration syringe to the nearest 0. Blood samples were collected immediately before and 6, 8, 24, 48, 72, and 96 hours after isotope administration. Enrichment of D 2 O and 18 O were determined in triplicate via isotope ratio mass spectrometry relative to standard mean ocean water isotopic standards. Thereafter, the equilibrated CO 2 was analyzed for 18 O enrichment. Isotope kinetic data were evaluated with a 2-pool model. The mean ± SD ratio of the dispersal space of D 2 O to that of H 2 18 O was calculated as 1. The DEE was estimated on the basis of the amount of CO 2 production by means of the RQ from open-flow indirect calorimetry of each cat and the calculated FQ expected o 2 and co 2 from oxidation of dietary protein, fat, and carbohydrates in the fed diet. Palmitate oxidation rate —Rate of fatty acid oxidation was estimated by determining the rate of flux or turnover of the 13 C-label in expired 13 CO 2 with a modification of the method reported by Wolfe. Because of its poor water solubility, in vitro combination of 1- 13 C-palmitate with albumin is customarily used to make the substance soluble for IV infusion in humans. This method requires an elaborate palmitate preparatory-extraction process and availability of an exogenous nonantigenic albumin source. To avoid antigenic sensitization of cats to heterologous albumin, a solubilization method was developed for the present study, with the solution of 1- 13 C-palmitate To prepare the 1- 13 C-palmitate infusion solution, blood samples 10 mL were collected from each cat by jugular venipuncture and subsequently warmed 37°C for 20 minutes to maximize clot retraction and platelet removal. Serum was harvested by centrifugation 1, × g for 15 minutes , heated 58° to 60°C for 15 minutes to inactivate complement and other proteases eg, thrombin , and then centrifuged 10, × g for 10 minutes. Thereafter, the solution was sonicated m and warmed via heat lamp to enhance and maintain palmitate solubility, cooled to room temperature approx 20°C , and filtered twice 0. A solution of NaH 13 CO 3 was prepared in 0. A priming dose of NaH 13 CO 3 p 2. Afterward, each cat received an IV infusion of 1- 13 C-potassium palmitate. l An infusion pump maintained a constant rate infusion for 90 minutes with the isotope suspension continuously mixed by means of a platform rocker. The 1- 13 C-palmitate infusions were performed in an isolated area to avoid cross contamination of the housing facility with the isotope. After 1- 13 C-palmitate had been infused for 60 minutes at a rate of 0. Expired gases were collected with a snug-fitting face mask and a 1-L gas-impenetrable latex rebreathing ventilation bag. q The apex end of the bag was fitted with an airtight 3-way stopcock that permitted syringe collection of expired gas. Breath samples were collected only after the bag was filled and emptied a minimum of 3 times. Collected gas samples were immediately injected into mL evacuated gas collection vials r and stored at room temperature until batched analyses. Isotope measurements were performed by means of source isotope-ratio mass spectrometry. s Plasma palmitate concentrations were measured in accordance with a standard method for FFA. in which Eb is the degree of enrichment of breath CO 2 , Ep is the degree of enrichment of palmitate in plasma, and k is correction factor for retention of bicarbonate in blood estimated as 0. Nitrogen balance —Degree of nitrogen balance was determined from the amount of nitrogen consumed in weighed food on a daily basis and the amount of nitrogen eliminated in urine and feces. Stoichiometric substrate oxidation rate —Estimates of substrate oxidation rates were made on the basis of indirect calorimetry gaseous exchange estimates and calculations according to the method of Frayn. in which 1 g of urinary nitrogen was assumed to reflect 6. Stoichiometric substrate calculations were completed for days 0, 42, and Statistical analysis —Summary statistics are reported as mean ± SD for normally distributed data or as median range for nonnormally distributed data. Box-and-whisker plots, histograms, and the Kolmogorov-Smirnov test were used to evaluate the data for a Gaussian distribution, with the aid of statistical software. t For intergroup comparisons, ANOVA for repeated measures or ANCOVA was used when data were normally distributed and Kruskal-Wallis ANOVA was used for other data fold increase in palmitate flux rate among diet groups. Differences in energy expenditure among groups were evaluated via ANCOVA, with DEE or REE as the dependent variable, diet and LBM as independent variables, and body weight as a covariate. Significant interactions of the independent variables with REE necessitated data transformation as described elsewhere. Differences in RQ were evaluated relative to baseline values within groups and relative to control group values for all cats that received carnitine on a per group and combined collective basis because of a concern that the small group size would limit the power to detect differences that truly existed. Two × 2 tables were used to evaluate differences between diet groups in cats achieving an IBW within the study period. Box-and-whisker plots were used to display range, median, and mean values for nonparametric data. Animals —With the exception of 1 cat in the control group that was removed from the study because of intractability, all cats completed the study. Diet groups were equivalent with respect to sex distributions, body weight, estimated IBW, and BCS before the diet trial began Table 1. Mean age in the groups were equivalent data not shown. Hematologic, serum biochemical, and urine analyses performed throughout the study did not reveal any abnormalities or signs that hepatic lipidosis had developed data not shown. For REE and RQ, 5 cats were censored from calculations involving day 84 data because those cats achieved targeted body weight between days 42 and 84 and were subsequently provided food allowances to maintain stable body weight. Energy ingestion during unrestricted and restricted feeding periods —Results of analysis of the weight reduction diets were summarized Table 2. No significant differences in daily food intake mass or energy were detected among groups during any phase of the study Table 3. See Table 2 for description of weight reduction diets. As expected, rapid rebound weight gain occurred with unrestricted feeding of the energy-dense diet days 85 to , with cats gaining a mean of 0. Some cats gained as much as 1. Percentage cumulative weight gain ranged from 6. Weight gain with ad libitum feeding of the energy-dense diet on days 85 to is represented as cumulative increase in body weight kg and as percentage increase of body weight on day Mean daily food consumption was 57 ± Mean daily energy ingestion was ± Daily energy expenditure was determined with doubly labeled water. Resting energy expenditure was measured by means of indirect calorimetry. The greatest weight loss in these cats occurred during days 43 to Five cats fed carnitine-supplemented diets achieved their target IBW before day 84 1 cat in the CN group, 1 in the CN group, and 3 in the CN group and had energy intake adjusted to maintain body weight thereafter. Adherence to study protocol resulted in censoring of indirect calorimetry data from these cats on day 84 because they were not continuing to undergo weight loss but were instead fed to maintain optimal body condition. Indirect calorimetry —No significant differences were detected among groups with respect to REE values at baseline Figure 1. Citation: American Journal of Veterinary Research 73, 7; That observation corresponded to findings during unrestricted access to the energy-dense diet fed during baseline and days and , compared with the restricted feeding of weight reduction diets days 1 to 84 , despite the higher fat content of the energy-dense diet. Cats that received no carnitine had mean RQs at baseline, day , and day of 0. Considering that baseline RQ reflected ingestion of a comparatively high-fat, energy-dense diet FQ, 0. The finding that the RQ had significantly decreased in cats that consumed carnitine-supplemented diets was further substantiated by the RQ increase in each carnitine-supplemented group upon restoration of unrestricted feeding of the higher fat energy-dense diet which was not carnitine supplemented from days through Palmitate oxidation —No significant differences were evident among diet groups in rates of palmitate flux or oxidation or estimated fatty acid appearance oxidation at baseline Figures 3 and 4. Rates of palmitate flux and estimated FFA oxidation were significantly higher on day 42 than at baseline in the unsupplemented, CN, and CN groups, as would be expected with weight loss. The onerous nature of the palmitate perfusion procedure precluded evaluations on more days than baseline and day Stoichiometric calculation of substrate oxidation —Stoichiometric calculation of substrate oxidation was limited to days in which LBM had been determined. With the exception of the CN group, there were no differences in estimated substrate oxidation between carnitine-supplemented and unsupplemented diet groups at baseline Figure 6. Median estimated fat oxidation rate at baseline in the CN group was However, the percentage increase in estimated fat oxidation in the control and CN groups were similar with median increases of This finding suggested that the group fed the unsupplemented diet maintained a higher rate of carbohydrate use, compared with the carnitine-supplemented groups. The present study involved several techniques to determine whether dietary l -carnitine supplementation during weight reduction alters fatty acid oxidation rate, REE, or LBM in overweight cats. Stable isotope methods estimating DEE and LBM were combined with indirect calorimetry and stable isotope labeled palmitate infusion to investigate metabolic responses. Few studies 30,31 have been conducted to investigate the influence of l -carnitine supplementation on fatty acid oxidation, and none have simultaneously measured energy expenditure and LBM or involved use of customized palmitate infusions as was done in the present study. Baseline measurements in the absence of supplemental l -carnitine were conducted before weight loss was initiated in the present study, and all variables for cats that received supplemental l -carnitine were compared over the study period with baseline measurements and measurements from a control group that received no supplemental carnitine. Also, because metabolic findings in the present study were compared with those obtained during feeding of a high-fat, energy-dense diet at baseline, it is probable that more extreme changes in fat oxidation and RQ would occur in similar studies of cats with stable body weights at baseline that receive a lower-fat, less energy-dense diet. Unrestricted feeding of the weight reduction diets achieved a weekly rate of weight loss ranging from 0. Initial diet acceptance with the abrupt dietary change was variable among cats, with some hesitant to eat the new diet during the first 2 to 7 days cats ate smaller amounts, but none failed to eat altogether. In most cats, quantitative consumption progressively increased over the 4 weeks of unrestricted feeding. In a few cats, there was little or no change in the amount of food ingested during the first week of diet introduction. The first weeks after diet introduction are believed to represent the period of highest risk for development of hepatic lipidosis in pet cats that are reluctant to consume the newly introduced food. To minimize this risk, gradual introduction of the new food by mixing it with the current food is generally recommended. Although the diet change was abruptly introduced in the present study, there was no evidence of an adverse effect on hematologic or biochemical variables secondary to reduced energy intake. Responses of the study cats to unrestricted feeding of the weight reduction diet suggested that this strategy may be used for initiating, sustaining, or transitioning cats with poor intake control glutonous feeding behavior to a more rigorous weight control program. As expected, unrestricted diet consumption still exceeded the daily energy allowances calculated to achieve weight reduction during the period the diet was fed. Mean weekly weight loss exceeded 1. There were no significant differences in rate of weight loss or total achieved weight loss between carnitine-supplemented and unsupplemented diet groups during feeding of the weight reduction diet. However, there were no significant differences between cats that did or did not receive the carnitine supplement. Therefore, collective findings regarding absolute weight reduction do not suggest an obvious benefit of dietary carnitine supplementation. The inconsistent response to dietary carnitine supplementation and the lack of a significant influence on weight loss and body condition change increased LBM , compared with findings in the control group, were at odds with the indirect calorimetry findings of a carnitine-enhanced rate of fatty acid oxidation. These disparate results might have been a result of limited statistical power too few cats , individual variation among cats, or a differing influence of carnitine-supplements given in amounts exceeding physiologic requirements. Although interpretation of change in gross body weight is complicated by the higher density and weight of muscle than in fat, change in LBM at endpoint of the weight reduction protocol was not different between the carnitine-supplemented and unsupplemented diet groups. Because LBM was determined by isotope dilution, it was only quantified on 3 days baseline and days 42 and 84 so that LBM could be used for REE normalization. A significant decrease in REE per LBM was observed only in cats fed the unsupplemented diet on days 42 and Whether that decrease reflected an influence of carnitine supplementation or individual variation remains to be substantiated through additional studies. An influence of adaptive thermogenesis in lowering REE during and after weight loss is a possible explanation, but this phenomenon remains controversial. Still other investigators have reported no detectable change in REE or DEE accompanying or after weight loss. Carnitine ingestion in the present study might have protected against adaptive thermogenesis as a means of sustaining metabolic rate. Consequently, the power to identify significant change in DEE among the diet groups, if it indeed existed, was low. Although metabolic effects of carnitine ingestion were variable and mild, cats fed the l -carnitine-supplemented diets sustained their REE per LBM kg , suggesting protection against adaptive thermogenesis during weight loss. This interpretation is supported by the finding of a significant reduction in RQ on day 42 in cats fed carnitine-supplemented diets and the consistently observed lower RQ in the combined analysis of all such cats relative to cats fed the unsupplemented diet throughout the restricted feeding period. Furthermore, upon reinstitution of unrestricted feeding of the energy-dense diet days 85 to , the REE increased in the control group, suggesting the observed difference from the other groups during the restricted-feeding phase of the study might have indeed been attributable to carnitine. The RQ significantly increased in all cats during reinstitution of unrestricted feeding of the energy-dense diet, despite the lower FQ relative to the weight reduction diet. This change in RQ consistent with a lower rate of fatty acid oxidation might simply have reflected cessation of weight loss or, alternatively, withdrawal of carnitine supplements. Food restriction resulted in a significant decrease in urinary nitrogen elimination, as expected, and there was no apparent influence of l -carnitine supplementation on nitrogen conservation. However, protein turnover rate was not specifically investigated. Weight reduction was associated with an increased percentage of palmitate oxidation and fatty acid flux rate estimated by 1- 13 C-palmitate infusions in each group, although values differed widely among individual cats. These findings also suggested that the diets supplemented with greater amounts of carnitine augment fatty acid oxidation. Several measured variables reflecting fatty acid oxidation rate during weight loss in overweight cats were investigated in the present study. Initial estimated rates of FFA turnover in cats at baseline were approximately 2- to 3-fold as great as those in humans 7. Although FFA appearance rates were in agreement with values previously reported for cats, 42,43 baseline values reflected consumption of the high-fat energy-dense diet as well as 12 hours of food restriction. Indirect calorimetry findings suggested that carnitine might protect against a decrease in metabolic rate in the presence of weight reduction and enhance in vivo fatty acid oxidation in overweight cats undergoing rapid weight reduction. However, the 13 C-palmitate infusion tests were unable to clearly demonstrate a similar carnitine effect, possibly because of the wide interindividual variability in palmitate oxidation. The final phase of the present study demonstrated the rapid rebound weight gain that may occur after substantial weight loss, upon reinstitution of unrestricted feeding of an energy-dense diet. |
| The Science behind Metabolism and L-Carnitine for Effective Fat Loss – Sova Health | Carnitine deficiency is rare in healthy people without metabolic disorders, indicating that most people have normal, adequate levels of carnitine normally produced through fatty acid metabolism. Two types of carnitine deficiency states exist. Primary carnitine deficiency is a genetic disorder of the cellular carnitine-transporter system that typically appears by the age of five with symptoms of cardiomyopathy, skeletal-muscle weakness, and hypoglycemia. Despite widespread interest among athletes to use carnitine for improvement of exercise performance, inhibit muscle cramps , or enhance recovery from physical training , the quality of research for these possible benefits has been low, prohibiting any conclusion of effect. The carnitine content of seminal fluid is directly related to sperm count and motility, suggesting that the compound might be of value in treating male infertility. Carnitine has been studied in various cardiometabolic conditions, indicating it is under preliminary research for its potential as an adjunct in heart disease and diabetes , among numerous other disorders. Although there is some evidence from meta-analyses that L-carnitine supplementation improved cardiac function in people with heart failure , there is insufficient research to determine its overall efficacy in lowering the risk or treating cardiovascular diseases. There is only preliminary clinical research to indicate the use of L-carnitine supplementation for improving symptoms of type 2 diabetes , such as improving glucose tolerance or lowering fasting levels of blood glucose. The kidneys contribute to overall homeostasis in the body, including carnitine levels. In the case of renal impairment , urinary elimination of carnitine increasing, endogenous synthesis decreasing, and poor nutrition as a result of disease-induced anorexia can result in carnitine deficiency. The form present in the body is l -carnitine, which is also the form present in food. Food sources rich in l -carnitine are animal products, particularly beef and pork. Humans endogenously produce 1. L-Carnitine, acetyl- l -carnitine , and propionyl- l -carnitine are available in dietary supplement pills or powders, with a daily amount of 0. Carnitine interacts with pivalate -conjugated antibiotics such as pivampicillin. Chronic administration of these antibiotics increases the excretion of pivaloyl-carnitine, which can lead to carnitine depletion. When taken in the amount of roughly 3 grams 0. Levocarnitine was approved by the U. Food and Drug Administration as a new molecular entity under the brand name Carnitor on December 27, Contents move to sidebar hide. Article Talk. Read Edit View history. Tools Tools. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item. Download as PDF Printable version. In other projects. Wikimedia Commons. Amino acid active in mitochondria. A16AA01 WHO l -form. US : OTC. IUPAC name. DB N. S7UI8SM58A R - - -: 0GFZZ9M Y. C Y. CHEBI Y. ChEMBL Y. Interactive image. Main article: carnitine biosynthesis. Further information: Systemic primary carnitine deficiency. Micronutrient Information Center, Linus Pauling Institute, Oregon State University, Corvallis, OR. Retrieved More research is needed to determine whether carnitine supplements affect male infertility or pregnancy rates in women with PCOS. Some research suggests that carnitine reduces levels of C-reactive protein, a biomarker of systemic inflammation, and levels of malondialdehyde, a lipid peroxidation product that induces pain and disability in patients with osteoarthritis [ 56 ]. In addition, levels of acylcarnitines conjugated carnitine esters are lower in people with osteoarthritis than in age- and gender-matched healthy individuals [ 57 ]. For these reasons, investigators are studying whether L-carnitine supplements can relieve osteoarthritis symptoms [ 56 , 58 ], but study results have been mixed. A randomized clinical trial examined the anti-inflammatory effects of L-carnitine supplementation for osteoarthritis management in 69 women age 40 to 60 years with mild to moderate osteoarthritis in both knees [ 59 ]. The women took mg L-carnitine three times a day or placebo for 8 weeks. Serum levels of several inflammation biomarkers and pain scores were lower in the carnitine group than in the placebo group: Interleukinbeta levels decreased 5. In comparison with placebo, carnitine did not reduce osteoarthritis pain or stiffness or increase physical function. Larger studies with samples that include both men and women are needed to determine whether carnitine supplementation helps manage osteoarthritis symptoms. Carnitine helps preserve muscle glycogen and promote fat oxidation. It also spares the use of amino acids as energy sources during exercise, making them potentially available for new protein synthesis [ 6 ], and decreases the accumulation of lactate [ 60 ]. However, research findings on the effectiveness of supplemental carnitine on athletic performance are mixed [ 6 ]. One study randomly assigned 14 recreational athletes age 24—28 years with an average body mass index BMI of 23 to consume a carbohydrate solution with or without 2. In another study, 24 men age 18—40 years eight omnivores and 16 vegetarians took 1 g L-carnitine twice daily for 12 weeks [ 62 ]. Carnitine supplementation had no significant effect on VO2max, blood lactate concentration, skeletal muscle energy metabolism, or physical performance in either the vegetarians or the omnivores. A comprehensive review summarized the effects of supplemental L-carnitine on exercise performance and recovery in well-trained athletes age 16—36 years and recreationally active adults age 18—50 years [ 63 ]. The review included 11 clinical trials one of which was the trial described above in a total of well-trained athletes who took 1 to 4 grams L-carnitine or placebo a single time or once or twice daily for up to 6 months. L-carnitine supplements reduced lactate levels and heart rate; increased lipid metabolism, VO2max, oxygen consumption, and L-carnitine plasma concentrations; improved performance; and hastened recovery in some of the studies. However, the supplements did not affect performance or maximal exercise test results in other studies. In 17 studies that included recreationally active adults, a total of participants took 2 g L-carnitine once or 2 to 4 g L-carnitine or placebo once or twice daily for up to 3 months. L-carnitine decreased plasma lactate concentrations, pyruvate concentrations, and muscle soreness and increased VO2max and recovery in some studies. However, in other studies, L-carnitine did not affect lactate, heart rate, VO2max, endurance, performance time, or perceived exertion during exercise. A systematic review of 11 randomized clinical trials examined the effects of oral L-carnitine supplementation on high- and moderate-intensity exercise performance in a total of physically active and untrained adults age 18 to 46 years [ 64 ]. The studies had mixed results. Some studies found significant improvements in VO2max, peak power, maximum sprinting power, perceived exertion, and number of repetitions and volume lifted in a leg press in the L-carnitine group. However, other studies found no differences in VO2max, fatigue, maximum and average power, or total work on a cycle ergometer. No studies found that L-carnitine supplementation improved moderate-intensity exercise performance. Because carnitine transports fatty acids into the mitochondria and acts as a cofactor for fatty acid oxidation, researchers have proposed using L-carnitine supplements to promote weight loss, often in conjunction with a low-calorie diet, exercise, or prescription weight-loss drugs [ 65 ]. Weight loss has been a secondary outcome in most studies, and these studies have had equivocal results. The trials included a total of participants. In eight trials, doses ranged from 1. Study participants who took carnitine supplements lost an average of 1. Carnitine does not have an established tolerable upper intake level. It can also cause muscle weakness in people with uremia and seizures in those with seizure disorders. Some research indicates that intestinal bacteria metabolize unabsorbed carnitine to form TMAO and gamma-butyrobetaine [ 68 ], which might increase the risk of CVD [ 38 , 39 , 69 , 70 , 71 ]. This effect appears to be more pronounced in people who consume meat than in vegans or vegetarians. The implications of these findings are not well understood and require more research. Several types of medications have the potential to interact with carnitine supplements. A few examples are provided below. People taking these and other medications on a regular basis should discuss their carnitine intake with their healthcare providers. Carnitine interacts with pivalate-conjugated antibiotics, such as pivampicillin, that are used to prevent urinary tract infections [ 72 ]. Chronic administration of these antibiotics can lead to carnitine depletion. However, although tissue carnitine levels in people who take these antibiotics may become low enough to limit fatty acid oxidation, no cases of illness due to carnitine deficiency in this population have been described [ 10 , 15 , 73 ]. Treatment with the anticonvulsants valproic acid, phenobarbital, phenytoin, and carbamazepine reduces blood levels of carnitine [ 74 , 75 , 76 , 77 ]. In addition, the use of valproic acid with or without other anticonvulsants may cause hepatotoxicity and increase plasma ammonia concentrations, leading to encephalopathy [ 76 , 78 ]. This toxicity may also occur after acute valproic acid overdoses. Intravenous L-carnitine administration might help treat valproic acid toxicity in children and adults, although the optimal regimen has not been identified [ 78 , 79 , 80 ]. For more information about building a healthy dietary pattern, refer to the Dietary Guidelines for Americans and the USDA's MyPlate. This fact sheet by the National Institutes of Health NIH Office of Dietary Supplements ODS provides information that should not take the place of medical advice. We encourage you to talk to your healthcare providers doctor, registered dietitian, pharmacist, etc. View More. 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