Productuon interfere with L-carnitine and energy production amd form of L-carnitine snergy may produce unwanted Building body resilience effects. In order to avoid the metabolic disturbance of estrogen during the sexual maturation of female fish, only male zebrafish 0. Diabetes Res Clin Pract. Yannicelli S, Rohr F, Warman ML: Nutrition support for glutaric acidemia type I.

L-carnitine and energy production -

The mitochondrial availability of carnitine during high-intensity exercise can be limited. After strenuous exercise, carnitine is believed to be a protective effect against muscle disruption.

It may help attenuate the release of creatine kinase and myoglobin. It may also help improve oxidative status and the protein signaling that is important for exercise recovery.

A review article by Gnoni and colleagues explored the potential role of L-carnitine supplementation in support of energy production during exercise. The authors describe a clinical trial where supplementation with 4 g of carnitine daily for 2 weeks in competitive walkers improved certain exercise-related parameters, including the maximum rate of oxygen consumption VO2max.

Other studies involving high performance athletes produced similar results. One study in junior athletes involved 1 g of carnitine supplementation for 6 weeks and reported higher athletic performances.

In untrained athletes , study participants experienced slight improvements in exercise performance in a study involving 2 g of carnitine daily for 2 weeks.

However, due to the relatively small sample size in these clinical trials, more research is needed to draw further conclusions. Carnitine plays other roles within the human body.

It has been shown to help support the transference of toxic compounds out of the mitochondria. It also may play a neuroprotective role. The acetyl derivative of L-carnitine, ALC, has been shown to pass through the blood-brain barrier at greater efficiency than L-carnitine.

ALC participates in glycogen synthesis, glucose metabolism modulation, increasing plasma adenosine triphosphate ATP concentration, and neurological function.

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Curr Eye Res. Stanley CA: Carnitine deficiency disorders in children. Download references. Institute for Eye Research, Sydney, New South Wales, Australia. School of Optometry and Vision Science, University of New South Wales, Sydney, Australia.

You can also search for this author in PubMed Google Scholar. Correspondence to Judith L Flanagan. The authors' responsibilities were as follows--QG and JLF conceived and researched the review; JLF drafted the review; QG, MDW, JV and PAS provided critical discussion and revision of the article for intellectual content, and approved the final version of the manuscript.

This article is published under license to BioMed Central Ltd. Reprints and permissions. Flanagan, J. et al. Role of carnitine in disease. Nutr Metab Lond 7 , 30 Download citation.

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Skip to main content. Search all BMC articles Search. Download PDF. Download ePub. Abstract Carnitine is a conditionally essential nutrient that plays a vital role in energy production and fatty acid metabolism. Introduction Carnitine β-hydroxy-γ- N -trimethylaminobutyric acid is widely distributed in food from animals sources but there is limited availability in plants [ 1 ].

Carnitine biosynthesis and metabolism Carnitine, a branched non-essential amino acid, is synthesized from the essential amino acids lysine and methionine.

Figure 1. Carnitine biosynthesis and metabolism. Full size image. Figure 2. Conclusion Carnitine as a nutritional supplement has, since the s, been promoted as beneficial in a number of disorders of human carnitine deficiency of impaired fatty acid oxidation, suggesting that nutritional or pharmacologic supplements of carnitine might be beneficial in some disorders [ ].

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BMC Cardiovasc Disord. Bakalov D, Sabit Z, Tafradjiiska-Hadjiolova R. Re: effect of l-carnitine supplementation on muscle cramps induced by stroke: a case report. Download references. Department of Human Physiology, Faculty of Health Sciences, Medical University of Gdansk, , Gdansk, Poland.

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Reprints and permissions. Sawicka, A. The bright and the dark sides of L-carnitine supplementation: a systematic review. J Int Soc Sports Nutr 17 , 49 Download citation. Received : 13 March Accepted : 04 September Published : 21 September Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Download ePub. Review Open access Published: 21 September The bright and the dark sides of L-carnitine supplementation: a systematic review Angelika K.

Olek ORCID: orcid. Abstract Background L-carnitine LC is used as a supplement by recreationally-active, competitive and highly trained athletes.

Methods A literature search was conducted in the MEDLINE via PubMed and Web of Science databases from the inception up February Results The initial search retrieved articles, and a total of 11 studies were finally included after applying inclusion and exclusion criteria.

Conclusion Prolonged LC supplementation in specific conditions may affect physical performance. Background The main function of L-carnitine LC is the transport of long-chain fatty acids into the mitochondrial matrix for their conversion in energy, via β-oxidation process [ 1 ]. Information sources and search The literature was explored using the MEDLINE via PubMed and Web of Science databases, including all articles published from the inception up February Study selection Firstly, studies were assessed by title verification between databases duplicates were removed.

Data collection process The following information was compiled for each study: authors, year of publication, type of study, length of supplementation, a dose of supplementation and main effect. Results Study selection By the above-described search strategy, publications were identified.

Flowchart on the search and selection of articles included in the review. Full size image. Table 1 Summary and results of the studies reviewed examining the LC supplementation Full size table.

Discussion The present findings have been debated in the six separate paragraphs, and for a better picture of LC supplementation, other studies were also disputed. Skeletal muscle protein balance regulation Skeletal muscle mass depends on the rates of protein synthesis and degradation.

Strengths and limitations The strength of this review is a focus on the period of LC treatment, very important aspect often missed in many articles dealing with this supplement. Conclusions Lasting for several years opinion that LC supplementation does not change metabolism, especially exercise metabolism, is based mostly on short-term supplementation protocols.

Availability of data and materials Not applicable. Abbreviations LC: L-carnitine TC: Total carnitine TMAO: Trimethylamine-N-oxide CHO: Carbohydrates IGF Insulin-like growth factor-1 PI3K: Phosphoinositidekinase Akt: Protein kinase B mTOR: Mammalian target of rapamycin S6K: S6 kinase 4E-BP: 4E-binding protein FoxO: Forkhead box O MuRF Muscle-specific RING finger-1 atrogin Muscle atrophy F-box mRNA: Messenger RNA BMI: Body mass index ROS: Reactive oxygen species.

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Carnitine is a quaternary Antibacterial body wash L-carnitine and energy production involved L-carnitine and energy production metabolism in most mammals, L-carhitine, and some bacteria. Some individuals with genetic or medical produchion L-carnitine and energy production as preterm infants cannot enerfy enough carnitine, requiring dietary supplementation. Many eukaryotes Mood enhancing lifestyle the ability to synthesize carnitine, including prdouction. HTML is then cleaved by HTML aldolase HTMLA, a pyridoxal phosphate requiring enzymeyielding 4-trimethylaminobutyraldehyde TMABA and glycine. Carnitine is involved in transporting fatty acids across the mitochondrial membrane, by forming a long chain acetylcarnitine ester and being transported by carnitine palmitoyltransferase I and carnitine palmitoyltransferase II. The tissue distribution of carnitine-biosynthetic enzymes in humans indicates TMLD to be active in the liver, heart, muscle, brain and highest in the kidneys. The rate of TMABA oxidation is greatest in the liver, with considerable activity also in the kidneys. Stress reduction properties, also L-carnitine and energy production L-carnitin levocarnitine, is a naturally occurring amino acid structure that Skin rejuvenation for uneven skin tone body produces. L-carnitine pgoduction a critical role in energy production, as it L-carnittine fat into energy. Those with low L-carnitine levels may benefit from taking an oral supplement, though. As well as supporting energy production, L-carnitine may help some other functions in the body, such as maintaining general brain function and reducing the risk of certain disorders. Some people may experience mild side effects when increasing their L-carnitine intake, especially with long-term use.

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In conclusion, ploidy significantly affected the energy metabolism in rainbow trout, dietary l -carnitine levels altered the l -carnitine homeostasis, but not influence nutritional metabolism.

Abdallah Tageldein Mansour, Ahmed H. Arisha, … Walaa El-Houseiny. Hirofumi Furuita, Tadao Jinbo, … Hideki Tanaka. Fish meal and fish oil derived from wild catches are dominant ingredients in aqua feed.

It is estimated, at the present annual growth rates, that fishmeal supplies will be entirely consumed by the aquaculture sector by Plant protein ingredients have increasingly been used in diets of aquaculture species Glencross Booth and Allan , including carnivore marine species Oliva-Teles and Gonçalves ; Colburn et al.

The replacement of fish meal may trigger, however, specific deficiency symptoms, including l -carnitine deficiency. Fishmeal may contain 10—20 times more l -carnitine than plant-based feeds Ozório et al. l -Carnitine, a multi-physiological and bioactive vitamin-like nutrient, plays an important role in cellular nutritional metabolic status, including the regulation of fish energy metabolism and growth Harpaz ; Mohseni et al.

Fish fed high-fat diets supplemented with mg l -carnitine showed a reduction in plasma glucose and lactate dehydrogenase LDH Ozório et al.

A decrease in LDH levels may also indicate an increase protection of l -carnitine against oxidative stress Ronca et al. According to Rasmussen and Wolfe growth is impaired when a dietary l -carnitine level is limited. In fish, an increase in energy demand is followed by the increase in lipid metabolism and body l -carnitine turnover Ozório et al.

Carnitine reserves are mainly replenished by the diet since carnitine biosynthesis is not sufficient, especially in very young animals Harpaz Ozório et al. juveniles fed l -carnitine supplements following acute exposure to toxic ammonia levels and to pathogen agent S. In case of fishmeal replacement, body l -carnitine reserves may become limited, thus dietary supplementation is required.

In salmonid production, sterile triploids have been increasingly used. After the onset of sexual maturation, triploid fish often grow faster and have better flesh quality than their diploid counterparts.

In addition, triploid fish may display greater hypertrophic growth and reduced energy costs for gamete production Thorgaard ; Qin et al. The comparative results between diploid and triploid fish are often contradictory Ihssen et al. The general consensus is that the survival and growth are substantially lower in the early life stages in triploids compared to diploids Thorgaard ; Sutterlin et al.

In addition, triploids appear to be less resilient and less tolerant to poor water quality than their diploid counterpart Benfey ; Benfey and Biron ; Altimiras et al. The aim of this study was to assess the effects of dietary l -carnitine levels on energy metabolism in diploid and triploid rainbow trout Oncorhynchus mykiss.

The current study is an extension of a published study Ozório et al. Two groups of 5-month-old rainbow trout were used, one of all-female diploid trout initial weight After an acclimatization period of 2 weeks, rainbow trout were individually weighed and randomly distributed in 18 fiberglass tanks of 50 L.

The water supply system consisted of a closed circuit TMC, TMC Iberia, Lisbon, Portugal , which included mechanical and biological filtration, a skimmer, an ultraviolet sterilization unit and a refrigerator.

The water quality parameters such as temperature Fish were fed twice daily and h , to apparent satiation. At the end of the trial all fish were starved for 24 h prior to sampling.

Before sampling, fish were euthanized by an overdose bath of 0. A total of 12 fish per group were sampled for muscle, liver and blood plasma analyses. The results of growth performance parameters are presented solely in the text of the Result section.

For detailed information about the growth performance, see Ozório et al. The voluntary feed intake VFI , feed conversion ratio FCR and growth rate daily growth index, DGI was calculated as follows:.

Diets, liver, and muscle tissues were analyzed for the free- and acyl l -carnitine content. All samples, prior to l -carnitine analysis, were deproteinated with perchloric acid, subsequently neutralized with potassium hydroxide, centrifuged and the supernatant collected.

l -Carnitine was extracted by stepwise heating, ultrasonic treatment or extraction with various detergents. Additionally, alkaline hydrolysis was performed for the determination of l -carnitine esters.

The l -carnitine determination in diets and tissues was performed by radiometric detection of free and l -carnitine esters. The assay is based on the reaction of free l -carnitine with acetyl-CoA catalyzed by carnitine acetyltransferase with the production of acetyl carnitine and coenzyme Christiansen and Bremer Blood was collected by caudal puncture with lithium-heparin coated syringes.

All plasma tests were performed in triplicate. The total ammonia concentration in plasma was determined using the method described by Bergmeyer and Beutler and plasma osmotic pressure mOsm was determined with an osmometer model 15—Löser Messtechnik, Berlin, Germany.

Plasma glucose concentrations were measured by the glucose oxidase method using a Beckman glucose analyzer 2 Beckman Instruments, Brea, CA, USA. Urea was quantified colourimetrically with the Glutamate dehydrogenase GLDH enzymatic method. Alanine aminotransferase ALT was quantified by an enzymatic method in accordance with IFCC.

Lactate dehydrogenase LDH was quantified by an enzymatic method in accordance with IFCC. All the methods were executed in a Roche Cobas Integra Chemistry Analyser Roche ® Sistemas de Diagnóstico, Amadora, Portugal , with Roche reagents.

Triiodothyronine T3 and thyroxine T4 were quantified by electrochemiluminescence immunoassays in a Roche Cobas e Analyser Roche ® Sistemas de Diagnóstico, Amadora, Portugal , with Roche reagents. All data were tested for normality using Kolmogorov—Smirnov and Levene tests and analyzed using two-way analyses of variance ANOVA.

The model included the effect of ploidy two levels and dietary l -carnitine three levels and their interaction. Data were analyzed using the General Linear Model procedure SAS Institute Inc.

Voluntary feed intake VFI: 1. Feed conversion ratio FCR: 0. Growth rate 2. The concentration of l -carnitine fractions free and acyl l -carnitine significantly increased in muscle and liver Fig. Free carnitine content was significantly higher than acyl l -carnitine content in both muscle and liver tissues.

Acyl l -carnitine, free l -carnitine and total carnitine content in muscle a and liver b of diploid and triploid rainbow trout fed the experimental diets. Ploidy and l -carnitine supplementation did not affect plasma glucose, urea, protein, and triglyceride levels Table 2. Trout fed mg l -carnitine had the lowest ammonia 8.

Plasma cortisol ranged from 4. In studies with larger animals, the positive effects of l -carnitine become less evident, as confirmed by Chatzifotis et al.

In the current study using juveniles, with exception of FCR, l -carnitine supplementation did not improve growth performance.

The ambiguity among many dose—response studies on l -carnitine may be caused by different l -carnitine concentrations, the husbandry conditions or the duration of the dietary treatment Ozório et al. The carnitine pool in animals is maintained by a combination of absorption of carnitine from supplemental sources, a modest rate of biosynthesis, and an efficient reabsorption of carnitine Rebouche and Seim The body distribution of carnitine is determined by a series of systems that transport carnitine into cells against a concentration gradient.

The liver plays a unique role in the whole-body carnitine homeostasis. Free and acyl l -carnitine content increased with the dietary l -carnitine supplementation, whereas higher levels were observed in muscle than in liver, indicating a direct relationship between the dietary and body l -carnitine.

The muscle may store a large amount of l -carnitine against a concentration gradient by an active transport process, which could be to ensure an immediate and efficient energy for the muscle during exercise and recovery.

The l -carnitine concentration gradient was even more pronounced between muscle and liver tissues Ozório et al. The ability to take up and retain dietary carnitine was observed in other species, such as Atlantic salmon Salmo salar L.

Ji et al. The increase in the acyl l -carnitine fraction in fish tissues may indicate an increase in lipid catabolism and that the diet quality and quantity may affect the body l -carnitine level. These results are consistent with the study described by Ozório et al. In fact, muscle l -carnitine levels increased moderately when African catfish were fed between 40 and mg l -carnitine.

Thereafter, a sharp increase in muscle l -carnitine level was observed. In the current study, the ploidy affected the acyl l -carnitine content in muscle, with higher values observed in triploid fish. This could indicate that triploid trout have higher l -carnitine requirement than diploid fish.

In fact, triploid fish have a lower respiratory efficiency and are more susceptible to stress than diploid fish. Triploid fish have fewer red blood cells which probably affect the exchange of oxygen and decrease the ability to transport oxygen in the blood Benfey ; Benfey and Biron ; Tiwary and Ray and, therefore, spend more energy to maintain internal balance than their diploid counterpart, possibly mobilizing more body l -carnitine for energy production.

Plasma lipase was higher in diploid fish and is in agreement with the slight increase in plasma triglyceride. Lipase is the rate-limiting enzyme for the hydrolysis of triglyceride in plasma Albalat et al.

In the current study, triploid trout had lower plasma ammonia concentrations, which may reflect on a higher capacity to excrete ammonia than diploid trout.

Considering that ammonia excretion rates are linked to acid—base regulation Kieffer and Tufts , triploid rainbow trout may have a greater clearance capacity of metabolic protons. This would allow for faster recovery from acidosis and energy ATP depletion after exercise, which is often the case during handling stress.

A faster recovery of the blood acid—base status may also reflect a faster recovery of ion and osmoregulatory imbalance, which was also shown by the significant differences in plasma osmolality between triploid and diploid trout. Plasma triiodothyronine hormone T 3 was significantly higher in diploid than triploid trout, as well as the feed intake VFI.

Feed intake, quality and quantity, is known to influence thyroid hormone levels in rainbow trout Leatherland et al. Thyroid hormones interact closely with the energy metabolism, with T 3 playing a role in the regulation of growth and nutrient partitioning in teleosts Peter and Marchant ; Korytko and Cuttler In the current study triploid trout had lower plasma LDH level.

As mentioned earlier, triploid fish have lower oxygen transport ability, which may explain their lower activity when compared to diploid trout. According to Sullivan and Somero , fish with different locomotors activity would have different LDH activity to compensate for the amount of lactate produced.

Wardle reported lower lactate ion concentration in flatfish than in rainbow trout. Although a multitude of questions concerning the regulation of dietary carnitine requirements remain to be elucidated, our study suggested that ploidy significantly affected the energy metabolism, whereas dietary l -carnitine levels altered the carnitine homeostasis, but did not influence energy metabolism in diploid and triploid rainbow trout.

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Elevated protein synthesis and attenuated proteolysis are observed during muscle hypertrophy. Both of these processes are mainly regulated by the signaling pathway: insulin-like growth factor-1 IGF-1 — phosphoinositidekinase PI3K — protein kinase B Akt — mammalian target of rapamycin mTOR.

The activation of mTOR leads to phosphorylation and activation of S6 kinases S6Ks and hyperphosphorylation of 4E-binding proteins 4E-BPs , resulting in the acceleration of protein synthesis. At the same time, Akt phosphorylates and inactivates forkhead box O FoxO , thereby inhibit the responsible for proteolysis ubiquitin ligases: muscle-specific RING finger-1 MuRF-1 and muscle atrophy F-box protein atrogin-1 , for review see [ 27 , 28 , 29 ].

The association between LC supplementation and the regulation of metabolic pathways involved in muscle protein balance have been shown in several animal studies Fig. Four weeks of LC supplementation in rats increased plasma IGF-1 concentration [ 33 ]. FoxO inactivation attenuated MURF-1 expression in quadriceps fem oris muscle of supplemented rats compared to control [ 33 ].

All these findings together might suggest that LC supplementation protect muscle from atrophy, especially in pathophysiological conditions. The association between LC supplementation and the regulation of metabolic pathways involved in muscle protein balance.

L-carnitine LC ; insulin-like growth factor-1 IGF-1 ; phosphoinositidekinase PI3K ; protein kinase B Akt ; mammalian target of rapamycin mTOR ; forkhead box O FoxO ; muscle-specific RING finger-1 MuRF-1 ; muscle atrophy F-box atrogin-1 ; increase ; decrease ; activation ; inactivation.

Various effects might be due to different IGF-1 levels; significantly lower in the HIV-seropositive patients than in healthy subjects [ 38 ]. These findings altogether suggest that prolonged LC supplementation might affect body composition in specific conditions.

Therefore, authors suggested that LC supplementation may be effective in obese and overweight subjects. It has been assumed that a combination of LC supplementation with increased energy expenditure may positively affect body composition.

However, either with aerobic [ 41 , 42 ] or resistance [ 43 ] training, LC supplementation has not achieved successful endpoint. Similarly, lack of LC effect has been reported in obese women [ 42 ]. Body composition, determined by dual energy X-ray absorptiometry, indicated no significant effect in fat mass and fat-free mass due to supplementation.

Moreover, LC administration did not influence bench press results. The number of leg press repetitions and the leg press third set lifting volume increased in the LC group compared to the placebo group [ 43 ].

Different LC effect in the limbs may be associated with the higher rates of glycogenolysis during arm exercise at the same relative intensity as leg exercise [ 44 ].

Aged people have accelerated protein catabolism, which is associated with muscle wasting [ 45 ]. LC could increase the amount of protein retention by inhibition of the proteolytic pathway. Six months of LC supplementation augmented fat free mass and reduced total body fat mass in centenarians [ 14 ].

Such effect was not observed in elder women age range 65—70 y. after a similar period of supplementation [ 15 ]. The effectiveness of LC supplementation may result from the age-wise distribution of sarcopenia.

The prevalence of sarcopenia increased steeply with age, reaching Muscle damage may occur during exercise, especially eccentric exercise. In the clearance of damaged tissues assist free radicals produced by neutrophils. Therefore, among other responses to exercise, neutrophils are released into the circulation.

While neutrophil-derived reactive oxygen species ROS play an important role in breaking down damaged fragments of the muscle tissue, ROS produced in excess may also contribute to oxidative stress for review see [ 47 , 48 ].

Based on the assumption that LC may provide cell membranes protection against oxidative stress [ 49 ], it has been hypothesized that LC supplementation would mitigate exercise-induced muscle damage and improve post-exercise recovery.

Since plasma LC elevates following 2 weeks of supplementation [ 21 , 22 ], short protocols of supplementation may be considered as effective in attenuating post-exercise muscle soreness. It has been shown, through magnetic resonance imaging technique that muscle disruption after strenuous exercise was reduced by LC supplementation [ 37 , 51 ].

This effect was accompanied by a significant reduction in released cytosolic proteins such as myoglobin and creatine kinase [ 50 , 52 , 53 ] as well as attenuation in plasma marker of oxidative stress - malondialdehyde [ 51 , 53 , 54 ].

Furthermore, 9 weeks of LC supplementation in conjunction with resistance training revealed a significant increase of circulating total antioxidant capacity and glutathione peroxidase activity and decrease in malondialdehyde concentration [ 43 ].

In Rebouche et al. Similar observations were noted in later human studies [ 56 , 57 ], with the peak serum TMAO observed within hours following oral administration of the tracer [ 56 ].

Prolonged LC treatment elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ]. Three months of oral LC supplementation in healthy aged women induced ten-fold increase of fasting plasma TMAO, and this level remained elevated for the further 3 months of supplementation [ 16 ].

Four months after cessation of LC supplementation, plasma TMAO reached a pre-supplementation concentration, which was stable for the following 8 months [ 60 ]. In Wang et al. Since diets high in red meat have been strongly related to heart disease and mortality [ 62 ], LC has been proposed as the red meat nutrient responsible for atherosclerosis promotion [ 8 ].

As a potential link between red meat consumption and the increasing risk of cardiovascular disease, TMAO has been indicated [ 8 ]. Numerous later studies have shown the association between increased plasma TMAO levels with a higher risk of cardiovascular events [ 63 , 64 , 65 , 66 ].

The recent meta-analyses indicated that in patients with high TMAO plasma level, the incidence of major adverse cardiovascular events was significantly higher compared with patients with low TMAO levels [ 67 ], and that all-cause mortality increased by 7.

The rise of plasma TMAO was on average three-fold compared with white meat and non-meat diets [ 70 ]. Conversely, habitual consumption of red, processed or white meat did not affect plasma TMAO in German adult population [ 71 ]. Similarly, a minor increase in plasma TMAO was observed following red meat and processed meat consumption in European multi-center study [ 72 ].

In the previous century, the underlined function of TMAO was the stabilization of proteins against various environmental stress factors, including high hydrostatic pressure [ 73 ]. TMAO was shown as widely distributed in sea animals [ 74 ], with concentration in the tissue increasing proportionally to the depth of the fishes natural environment [ 75 ].

Consequently, fish and seafood nutritional intake has a great impact on TMAO level in the human body [ 76 ], significantly elevating also plasma TMAO concentration [ 72 ]. Therefore, link between plasma TMAO and the risk of cardiovascular disease [ 8 ] seems like a paradox, since more fish in the diet reduces this risk [ 77 ].

Not only dietary modification may affect TMAO plasma levels. Due to TMAO excretion in urine [ 56 , 57 ], in chronic renal disease patients, TMAO elimination from the body fails, causing elevation of its plasma concentration [ 78 ]. Therefore, higher plasma TMAO in humans was suggested as a marker of kidney damage [ 79 ].

It is worthy to note that cardiovascular disease and kidney disease are closely interrelated [ 80 ] and diminished renal function is strongly associated with morbidity and mortality in heart failure patients [ 81 ].

Moreover, decreased TMAO urine excretion is associated with high salt dietary intake, increasing plasma TMAO concentration [ 82 ]. The relation between TMAO and chronic disease can be ambiguous, involving kidney function [ 79 ], disturbed gut-blood barrier [ 83 ], or flavin-containing monooxygenase 3 genotype [ 84 ].

Thus, whether TMAO is an atherogenic factor responsible for the development and progression of cardiovascular disease, or simply a marker of an underlined pathology, remains unclear [ 85 ].

Carnitine preparations administered orally can occasionally cause heart-burn or dyspepsia [ 86 ]. It is worthy to mention that Bakalov et al. The strength of this review is a focus on the period of LC treatment, very important aspect often missed in many articles dealing with this supplement.

This limitation is also magnified by the varied design of the studies available including different supplementation protocols and outcome measures. There is also a high degree of heterogeneity among participants of the analyzed studies. Therefore, the results should be taken with caution, and more research is required before definitive recommendations.

Lasting for several years opinion that LC supplementation does not change metabolism, especially exercise metabolism, is based mostly on short-term supplementation protocols. Nevertheless, LC is still used by elite [ 9 ] and sub-elite [ 10 ] athletes. Recent studies suggest that LC supplementation may elevate muscle TC content; therefore, modify muscle fuel metabolism and performance during the exercise.

Due to insulin-mediated LC transport to the muscle, oral administration regimen should be combined with CHO. Because of LC poor bioavailability, it is likely that the supplementation protocol would take at least 3 months. Shorter period of supplementation may be effective in prevention of exercise-induced muscle damage, but not metabolic changes.

On the other hand, it is also clear that prolonged LC supplementation elevates fasting plasma TMAO [ 16 , 17 , 18 , 58 , 59 ], compound supposed to be pro-atherogenic [ 61 ]. Therefore, additional studies focusing on long-term supplementation and its longitudinal effect on the TMAO metabolism and cardiovascular system are needed.

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Some studies an it may produuction some health benefits, including increased energt loss, improved brain Clarifying nutrition myths, and more. Ane is used for weight L-carnitine and energy production and may have an impact on brain function. This article examines the potential risks and benefits of L-carnitine supplements and explains how this nutrient functions in your body. L-carnitine is a nutrient and dietary supplement. The mitochondria act as engines within your cells, burning these fats to create usable energy.