Dietary Carnitine Supplementation Research Articles

Effects of dietary carnitine supplementation on semen output and quality of boars

Carnitine is an amino acid derivative that performs the functions of increasing energy production as well as acting as an antioxidant for sperm cells. This study was conducted to investigate the effects of the inclusion of carnitine in boar diets on semen output and quality. Sixty-four purebred and hybrid boars at a commercial boar stud were blocked by age and semen quality and randomly allotted to receive a daily 30 g top-dress of either soybean meal (CON) or soybean meal and 625 mg of L-Carnitine (CARN). Supplementation lasted for 12 weeks from May to July 2021 during which weekly semen collection was performed. Semen was evaluated in the stud for concentration and motility parameters using computer-assisted semen analysis (CASA). Samples were shipped to Purdue University for detailed morphology, viability, and CASA analysis performed in samples stored at 17 °C for 5 days. PROC Mixed (SAS v 9.4) was used to analyze data, with boar nested within treatment used in repeated measures analysis. Semen quality estimates from the week before supplementation were used as covariates in the statistical model. Tukey-Kramer adjustment was used for means separation. Carnitine supplementation had no effects on total sperm produced (P = 0.35). Percentage of motile sperm cells (P = 0.63), morphologically normal sperm (P = 0.42), viable sperm (P = 0.43), or sperm with normal acrosomes (P = 0.61) in the ejaculates were not different among treatments. Sperm kinematics in CARN ejaculates tended to have greater straight-line velocity and distance (P = 0.06 and P = 0.07, respectively). There were several interactions of treatment and day of storage for the kinematic parameters. However, these interactions do not show observable trends for CARN to improve or depress sperm function. Overall, the inclusion of 625 mg/d of carnitine in the diet of boars for 12 weeks had no effects on sperm output or quality with minor changes to sperm cell kinematics.

PSIII-9 Effects of Dietary Carnitine Supplementation on Semen Output and Quality in Boars

Abstract Carnitine is an amino acid derivative with functions in increasing energy production as well as acting as an antioxidant for sperm cells. The objective of this study is to investigate the effects of the inclusion of carnitine in boar diets on sperm output and quality. Sixty-four boars at a commercial boar stud were blocked by age and semen quality and randomly allotted to receive a daily 30 g top-dress of either corn (CON) or corn and 625 mg of carnitine (CARN). Supplementation lasted for 12 weeks from May-July, 2021 during which weekly semen collection was performed. Semen was evaluated at the stud for concentration and motility parameters using computer-assisted semen analysis (CASA). Samples were also shipped to Purdue University for detailed morphology, viability, and CASA performed in samples stored at 17C for 5 d. PROC Mixed (SAS v 9.4) was used to evaluate the data where boar nested within treatment was used in repeated measures with the main effects of treatment and week and semen quality estimates from the week prior to supplementation as covariates in the model. Carnitine supplementation had no effects on total sperm produced (P = 0.35). Percentage of motile sperm cells (P = 0.38), morphologically normal sperm (P=0.42), viable sperm (P = 0.43), or sperm with normal acrosomes (P = 0.61) in the ejaculates was not different among treatments. Sperm kinematics in CARN ejaculates tended to have greater straight-line velocity and distance (P = 0.06 and P = 0.07, respectively). There were several interactions of treatment and day of storage for the kinematic parameters, however, these interactions do not show an observable trend for CARN to improve or depress sperm function. Overall, the inclusion of 625 mg/d of carnitine to the diet for 12 weeks had no effects on sperm output or quality with minor changes to sperm cell kinematics.

Preventive Role of L-Carnitine and Balanced Diet in Alzheimer's Disease.

The prevention or alleviation of neurodegenerative diseases, including Alzheimer’s disease (AD), is a challenge for contemporary health services. The aim of this study was to review the literature on the prevention or alleviation of AD by introducing an appropriate carnitine-rich diet, dietary carnitine supplements and the MIND (Mediterranean-DASH Intervention for Neurodegenerative Delay) diet, which contains elements of the Mediterranean diet and the Dietary Approaches to Stop Hypertension (DASH) diet. L-carnitine (LC) plays a crucial role in the energetic metabolism of the cell. A properly balanced diet contains a substantial amount of LC as well as essential amino acids and microelements taking part in endogenous carnitine synthesis. In healthy people, carnitine biosynthesis is sufficient to prevent the symptoms of carnitine deficiency. In persons with dysfunction of mitochondria, e.g., with AD connected with extensive degeneration of the brain structures, there are often serious disturbances in the functioning of the whole organism. The Mediterranean diet is characterized by a high consumption of fruits and vegetables, cereals, nuts, olive oil, and seeds as the major source of fats, moderate consumption of fish and poultry, low to moderate consumption of dairy products and alcohol, and low intake of red and processed meat. The introduction of foodstuffs rich in carnitine and the MIND diet or carnitine supplementation of the AD patients may improve their functioning in everyday life.

Growth Performance, Biochemical Indices and Antioxidant Status of Grey Mullet (Mugil cephalus Linnaeus, 1758) Under Dietary L-Carnitine Supplementation

The present research evaluated the use of dietary carnitine supplementation and its effects on the growth, body composition, fatty acids, biochemical parameters, Insulin-like growth factor 1 (IGF-1) level and antioxidant activity, in grey mullet. Four experimental diets were prepared by adding carnitine at concentrations of 0, 400, 800, and 1200 mg kg−1 diet (C0, C400, C800 and C1200 respectively). After 9 weeks of the feeding trial, a significant increase in growth performance (except for Daily Growth Rate or DGR), carcass quality (crude protein and crude lipid), biochemical parameters (cholesterol, triglyceride, total lipid, free fatty acid or FFA, total protein, albumin, and globulin), plasma superoxide dismutase and glutathione peroxidase activities was detected in the fish fed on C800 diet, as compared to those fed on the other diets (P 0.05) differences were observed in moisture and crude ash contents among groups. Barring the C1200 diet, there was also a positive correlation between the plasma IGF-1 level and DGR. The results showed that the diet containing 800 mg kg−1 L-carnitine enhanced growth yield, feed utilization, and carcass quality; as well as biochemical and antioxidant activity of grey mullet. The authors concluded that the maximum recommended levels of L-carnitine in diets for grey mullet (Mugil cephalus) can be established at 800 mg kg−1.

Dietary L-carnitine supplementation increases lipid deposition in the liver and muscle of yellow catfish (Pelteobagrus fulvidraco) through changes in lipid metabolism.

Carnitine has been reported to improve growth performance and reduce body lipid content in fish. Thus, we hypothesised that carnitine supplementation can improve growth performance and reduce lipid content in the liver and muscle of yellow catfish (Pelteobagrus fulvidraco), a commonly cultured freshwater fish in inland China, and tested this hypothesis in the present study. Diets containing l-carnitine at three different concentrations of 47 mg/kg (control, without extra carnitine addition), 331 mg/kg (low carnitine) and 3495 mg/kg (high carnitine) diet were fed to yellow catfish for 8 weeks. The low-carnitine diet significantly improved weight gain (WG) and reduced the feed conversion ratio (FCR). In contrast, the high-carnitine diet did not affect WG and FCR. Compared with the control diet, the low-carnitine and high-carnitine diets increased lipid and carnitine contents in the liver and muscle. The increased lipid content in the liver could be attributed to the up-regulation of the mRNA levels of SREBP, PPARγ, fatty acid synthase (FAS) and ACCa and the increased activities of lipogenic enzymes (such as FAS, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and malic enzyme) and to the down-regulation of the mRNA levels of the lipolytic gene CPT1A. The increased lipid content in muscle could be attributed to the down-regulation of the mRNA levels of the lipolytic genes CPT1A and ATGL and the increased activity of lipoprotein lipase. In conclusion, in contrast to our hypothesis, dietary carnitine supplementation increased body lipid content in yellow catfish.

Boosting fat burning with carnitine: an old friend comes out from the shadow

Understanding the regulation of fuel utilization has been a topic of great interest and has practical implications to athletic performance and to prevention of pathophysiological metabolic conditions. The balance between carbohydrates (CHO) and lipids is regulated by a complex system with multi-site feedback and feedforward control as well as interaction between the pathways. Carnitine has a crucial role in lipid oxidation by mediating the translocation of long-chained fatty acids into mitochondria. During the past 30 years, dietary supplementation with carnitine has been widely used in order to enhance lipid oxidation and increase exercise performance. The evidence for an ergogenic effect of carnitine is, however, limited and most studies show no effect of carnitine supplementation on lipid oxidation. This is hardly unexpected since there is hitherto no evidence that muscle carnitine content can be increased by carnitine feeding in healthy men. In a recent issue of The Journal of Physiology, Wall and colleagues were able to show for the first time that muscle carnitine can be increased in healthy men by dietary carnitine supplementation (Wall et al. 2011). The same research group led by Paul Greenhaff has shown in a previous study that 6 h intravenous infusion with a combination of carnitine and insulin elevated muscle carnitine by 13% (Stephens et al. 2006). The mechanism is probably related to stimulation by insulin of the Na+-coupled transmembrane carnitine transport and is the theoretical foundation for the present study, where carnitine feeding was combined with CHO. Three months of dietary supplementation with a combination of carnitine and CHO had no effect, but after 6 months muscle carnitine content increased by 21%. The necessity of using a very long supplementation period demonstrates the difficulties involved and explains the failure of previous studies with shorter intervention periods. In this work, they have not only shown increased muscle carnitine but also that this alters muscle metabolism during exercise. Firstly, during low-intensity exercise (50%) carnitine supplementation resulted in reduced glycogen utilization and reduced activity of the pyruvate dehydrogenase complex (PDC). PDC is a main control point of CHO oxidation and has a complex mode of control including feedback inhibition by the products acetyl-CoA and NADH (Fig. 1). The investigators suggest that the reduced PDC activity is due to a carnitine-mediated increase in lipid-derived acetyl-CoA. Although this explanation is consistent with theoretical models (Randle et al. 1963) the current data give limited experimental support in that the acetyl-carnitine/carnitine ratio, which reflects the acetyl-CoA/CoA ratio, was lower after carnitine supplementation. The carnitine-induced sparing of muscle glycogen is an important finding and is consistent with an increased lipid oxidation. However, an obvious limitation of this study is that there are no measurements of lipid oxidation, which should have been one of the primary outcomes. Another finding in this work, was that at high-intensity exercise (80%) muscle lactate was reduced after carnitine supplementation. Simultaneously PDC activity was increased, i.e. opposite to that observed during low-intensity exercise. The increased PDC activity was explained by the role of carnitine in buffering acetyl-groups giving rise to reduced levels of the PDC inhibitor acetyl-CoA. The lower muscle lactate after carnitine supplementation suggests a better matching between glycolytic flux and CHO oxidation. Carnitine supplementation also had an ergogenic effect and was shown to increase work output by 11% in a performance trial with a fixed duration of 30 min. The ergogenic effect was explained by the dual role of carnitine – glycogen sparing at low intensities and reduced muscle lactate accumulation at high intensities. This well controlled study by Wall et al. 2011, has broad implications. An important and robust finding is that muscle carnitine can be increased by dietary means in subjects without carnitine deficiencies and that this has a clear influence on muscle metabolism and performance. The results may have significant implications for athletic performance but the requirements of long-term treatment will most likely restrict the use of carnitine as an ergogenic aid. The results may also have some clinical importance in the treatment of type 2 diabetes and other metabolic diseases, which are related to a deteriorated lipid metabolism. It may be anticipated that further work on this subject will determine whether carnitine can specifically enhance lipid oxidation.

Effects of dietary methionine levels and L-carnitine supplementation on performance and egg quality parameters of layers

Effects of dietary carnitine supplementation (0 and 150 mg/kg L-carnitine) on performance and egg quality parameters of layers in late laying period (from 62 to 72 weeks) fed maize-soyabean meal based diets with different methionine levels (0.26 vs 0.40%) were investigated. A RCBD with 2×2 factorial arrangement was applied. Eight replicates of the four dietary treatments (3 layers in each cage, a total of 32 cages) were randomly distributed into blocks. The study period was 10 weeks and ninety six 62-week-old Nick Chick white layers were used. In the study, dietary carnitine supplementation did not affect egg production, feed consumption and feed efficiency. However, dietary methionine below requirement level either numerically (the first 5 week from 62 to 67th weeks and overall 10-week period) or statistically (P<0.05) (last 5 week from 67 to 72th weeks) reduced egg production and feed efficiency. Similar to performance data, dietary carnitine supplementation had no impact on egg, egg yolk, and egg shell weights, however, the reduction in dietary methionine level had negative impacts on these parameters as early as 4th week of the study. Neither carnitine nor methionine improved corrected yolk and egg shell weight, yolk colour and egg shell thickness, however, both egg shape index and Haugh unit were affected by dietary methionine levels (P<0.05). In summary, carnitine supplementation did not affect layer performance and egg quality whereas dietary methionine deficiency significantly reduced layer performance and egg quality in late laying period and the effect was more visible towards the end of the study.

Carnitine and type 2 diabetes

Studies in humans and animals demonstrate that "lipid over supply" causes or worsens insulin resistance via multiple mechanisms involving the accumulation of intracellular lipids in multiple tissues. In particular, the accumulation of fatty acyl CoA derivatives/metabolites in muscle inhibits both insulin signaling and glucose oxidation. Therefore agents that ameliorate the accumulation of fatty acyl CoA derivatives and/or their metabolites would be beneficial in the treatment or prevention of insulin resistance and T2D. Hyperinsulemic/euglycemic clamp studies in humans and carnitine supplementation studies in rodents provide "proof-of-concept" that carnitine is effective at improving insulin-stimulated glucose utilization and in reversing abnormalities of fuel metabolism associated with T2D. Carefully controlled clinical trials are warranted to determine the efficacy dietary carnitine supplementation as an adjunctive treatment for type 2 diabetes.

Dietary L-Carnitine Supplementation to Cultivated Fish: A Mini-Review

It is not clear whether animals require exogenous carnitine, and over the past 20 years, the scientific discussion regarding this subject continued with arguments pro and contra. Some studies observed that feeding fish with dietary carnitine supplements may improve growth and protect against several disease outbreak. However, such growth improvement was not always observed. The results can be interpreted in two ways: Firstly, the endogenous carnitine biosynthesis may be adequate to maintain sufficient tissue levels during growth. Secondly, the responses to dietary carnitine supplements are influenced by environmental and physiological interactions. The aim of this mini review was to provide an overview of the positive effects of dietary carnitine supplementation on fish metabolism, and possible factors that might alter dietary carnitine requirements, such as feed composition, species, age, tissue dependence on fatty acid oxidation and metabolic conditions.

Dietary canitine maintains energy reserves and delays fatigue of exercised african catfish (Clarias gariepinus) fed high fat diets

Lipids, together with proteins, are traditionally considered as primary fuels during aerobic swimming. The effects of dietary fat and carnitine supplements and exercise on the energy metabolism of juvenile fish were investigated. One hundred African catfish (Clarias gariepinus) were fed four isonitrogenous diets containing a fat level of 100 or 190 g kg-1 diet and one of the two levels of carnitine (15 and 1000 mg kg-1). Fish grew from 61 to 162 g in 10 wk. Thereafter, 6 fish per group swam vigorously for 3 h and the results were compared with unexercised groups. Fish receiving 1,000 mg carnitine accumulated 2- to 3-fold more carnitine than fish receiving 15 mg carnitine. Plasma acyl-carnitine level was affected by an interaction between dietary treatment and exercise (P &lt; 0.05). Adenosine triphosphate and phosphocreatine concentrations were higher in the white muscle (WM) of exercised fish fed the high-carnitine supplements, compared with the low-carnitine fed fish (P &lt; 0.05). Adenilate energy charge indexes were higher and ammonia concentrations were lower in WM of fish fed high-carnitine and high-fat diets. Dietary carnitine supplements may be needed in growing fish when dietary lipid level is high. In that case extra dietary carnitine can maintain the body energy reserves at adequate level when fish is exposed to a short-term, exhaustive exercise, a physiologic stress common both in nature and in intensive aquaculture systems.

Effects of dietary carnitine and protein energy:nonprotein energy ratios on growth, ammonia excretion and respiratory quotient in African catfish,Clarias gariepinus(Burchell) juveniles

Two separate feeding experiments were carried out to determine the effects of dietary carnitine supplements on growth rates, total ammonia nitrogen (TAN) excretion and respiratory quotient rates (RQ) in the African catfish, Clarias gariepinus (Burchell), juveniles fed various diets differing in protein energy:nonprotein energy ratio (PE:NPE). In Experiment 1, 540 fish (20.9 ± 1.0 g) were evenly distributed into six dietary groups and fed in duplicate aquaria (N = 12 aquaria) to apparent satiation over a 41-day period, until all fish attained an individual final weight of 156.9 ± 10.8 g. Diets were formulated to contain two levels of carnitine (80 and 660 mg kg−1) and three levels of PE:NPE (0.7, 0.9 and 1.4). Sampling was divided into two size ranges, according to the predicted individual end-weight of 60 g (days 0–16) and 160 g (days 16–41). In Experiment 2, 240 fish (16.5 ± 0.2 g) were distributed in four 140-L aquaria connected to a respirometer and preconditionally fed twice a day at a restricted feeding level of 24 g kg−0.8 day−1 for a 25-day period (final weight of 77.5 ± 1.5 g). Four isonitrogenous diets (368 g kg−1 crude protein) were formulated to contain two levels of fat (85 and 175 g kg%−1) and two levels of carnitine (40 and 600 mg kg−1), in a 2 × 2 factorial design. From days 20–25, three respirometric trials were carried out, during which total ammonia nitrogen (TAN) and RQ were determined over 24 h. In both experiments, carnitine supplemented fish accumulated 2.5−4 times more carnitine in their tissues than fish fed a basal level (P < 0.05). In Experiment 1, the smallest fish (<60 g) fed 660 mg carnitine showed significantly higher growth rates and lower feed conversion rates than 80 mg carnitine supplemented fish only when the dietary PE:NPE ratio was low (0.7). Additionally, dietary carnitine significantly increased protein:fat ratios in the whole body, suggesting a protein-sparing action. In Experiment 2, high carnitine supplements decreased both TAN excretion and RQ rates in fish <80 g.

Changes in fatty acid concentrations in tissues of African catfish, Clarias gariepinus Burchell, as a consequence of dietary carnitine, fat and lysine supplementation.

A study was undertaken to examine the effect of different dietary carnitine (200 and 1000 mg/kg diet) and fat (90 and 190 g/kg diet) supplementation on growth and fatty acid concentrations of fish fed either with a low- (13 g/kg) or a high-lysine (21 g/kg) diet. African catfish (22.7 g/fish), Clarias gariepinus Burchell, juveniles were stocked (sixteen aquaria, twenty-five fish per aquarium) and fed for a maximum of 74 d. Dietary lysine had a clear effect on growth performance and feed conversion ratios, but dietary carnitine supplements had no effect. High-carnitine supplements increased total carnitine content (P<0.0004) and reduced tissue free carnitine: acyl-carnitine ratio (P<0.05) compared with low-carnitine supplements. High-fat supplements decreased liver carnitine concentrations. Clear effects on liver fatty acid concentrations were observed in high-carnitine-fed fish compared with low-carnitine-fed fish. The primary liver fatty acids affected were n-6 (linoleic acid), n-3 (eicosapentanoic acid) and n-3 (docosahexanoic acid). The whole-body fatty acid balance suggested that n-3 disappeared (apparently by beta-oxidation) more readily than n-6 and/or n-3. From 774 mg n-3 eaten by high-lysine-high-fat-low-carnitine fish, 58 % was not assimilated into body tissues. High-carnitine-fed fish showed an increase in n-3 oxidation by 7 % compared with low-carnitine fish. Although dietary carnitine did not improve body growth, these results support the hypothesis that carnitine can enhance the mobilisation of long-chain fatty acids towards oxidation.

L‐carnitine supplementation and lipid metabolism of rats fed a hyperlipidaemic diet

SummaryUntil now, there has been no clear knowledge about the effect of dietary carnitine supplementation on lipid metabolism. Therefore, this study was conducted to investigate the effect of a dietary l‐carnitine supplementation (500 mg/kg) onx the lipid metabolism of adult rats. Rats fed a hyperlipidaemic basal diet containing 15% lard and 1% cholesterol were used as an animal model. The feeding period was 6 weeks. As parameters of lipid metabolism, the concentrations of individual lipids in plasma, lipoproteins and liver and the fatty acid composition of liver and erythrocyte total lipids were determined. There were no significant differences between the control group and the group receiving the diet supplemented with carnitine on parameters of animal performance (daily body weight gains and feed conversion ratio). As expected, plasma, very low‐density lipoproteins (VLDL) and liver exhibited high concentrations of cholesterol. Concentrations of triglycerides and phospholipids in plasma and individual lipoproteins as well as the concentrations of triglycerides, cholesterol and phospholipids in the liver were not significantly altered by dietary carnitine supplementation. The concentration of cholesterol in plasma and liver was increased by dietary carnitine. The fatty acid composition of liver and erythrocyte total lipids was not influenced by dietary carnitine supplementation. In conclusion, this study does not indicate a lipid‐lowering effect of dietary carnitine supplementation in hyperlipidaemic rats. Probably, the essential functions of carnitine in metabolism were realized by carnitine which was synthesized endogenously.

Modulation of nerve growth factor internalization by direct interaction between p75 and TrkA receptors.

While the central role played by TrkA in nerve growth factor (NGF) signalling has been established by dissecting its signal transduction pathways, insight into the mechanism of action of p75LNR, the low-affinity neurotrophin receptor, has only recently been achieved. The relative contribution of p75LNR and TrkA to the constitution of high-affinity receptors for NGF and, similarly, with TrkB an TrkC to the formation of those for other neurotrophins, is presently under debate. Some form of collaboration in mediating neurotrophin activities has been observed between the Trk and p75LNR receptors, but only recent indirect evidence indicates a molecular interaction. In the present work, we have ectopically coexpressed p75LNR and TrkA in Sf9 insect cells by using baculovirus vectors, and show a direct association between the two NGF receptors. In addition, we show that the intracellular and extracellular domains of both receptors contribute to this interaction. Finally, we demonstrate that NGF becomes endocytosed in TrkA-expressing cells but not in p75LNR-expressing cells, and that such function can be modulated by the presence of the intracellular domain of p75LNR receptor.

Dietary carnitine supplements slow disease progression in a putative mouse model for hereditary ceroid-lipofuscinosis

The childhood ceroid-lipofuscinoses are a group of autosomal recessively inherited disorders characterized by massive accumulation of autofluorescent lysosomal storage bodies in neurons as well as other cell types. The storage body accumulation is accompanied by severe degeneration of the central nervous system that results in blindness, cognitive and psychomotor degeneration, and premature death. On the basis of pathologic and biochemical criteria, a hereditary disease in the mnd mouse strain has been proposed as a model for certain types of human ceroid-lipofuscinosis. Experimental evidence suggests that the storage body accumulation in humans with juvenile and late-infantile ceroid-lipofuscinosis is linked to altered carnitine biosynthesis. On the basis of the latter observation, a study was performed to determine whether dietary carnitine supplements could slow the disease progression in the mnd mouse model. Carnitine supplementation begun at 4 weeks of age did not slow the retinal degeneration that is characteristic of this disease. It did, however, significantly elevate brain carnitine levels, slow the accumulation of autofluorescent storage bodies in brain neurons, and prolong the lifespans of the treated animals. These findings suggest that there is a link between carnitine biosynthesis and the disease pathology and indicate that carnitine supplementation may be beneficial in slowing the disease progression in humans with certain types of hereditary ceroid-lipofuscinosis. J. Neurosci. Res. 50:123–132, 1997. © 1997 Wiley-Liss, Inc.

Dietary carnitine supplements slow disease progression in a putative mouse model for hereditary ceroid‐lipofuscinosis

Dietary carnitine supplements slow disease progression in a putative mouse model for hereditary ceroid‐lipofuscinosis

The Effect of Dietary Carnitine Supplementation on Growth of Rainbow Trout Fingerlings

The Effect of Dietary Carnitine Supplementation on Growth of Rainbow Trout Fingerlings

The effect of dietary carnitine supplementation on growth of red sea bream ( Pagrus major) fingerlings at two levels of dietary lysine

The effect of dietary carnitine supplementation (2 g kg −1 diet) on growth, proximate, neutral lipid and fatty acid composition of liver and muscle of red sea bream fingerlings at two levels of dietary lysine (10 and 14 g kg −1 diet, respectively) was investigated. Carnitine increased red sea bream growth fed a 14 g lysine kg −1 diet ( P < 0.05) but did not cause any effect on growth in fish fed the 10 g lysine kg −1 diet. A clear lysine sparing effect of carnitine in red sea bream was not observed. Carnitine did not reduce crude lipid levels in white muscle and liver of fish. Fatty acid composition of total lipids in liver showed reduced values for eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and total long-chain fatty acids with 20 to 24 carbon atoms (ΣC 20–24) in fish receiving carnitine supplemented diets indicating an increased utilization of the above fatty acids. Free carnitine and acid-soluble carnitine in muscle increased two-fold after carnitine administration.

Ruminal Degradation and Dose Response of Dairy Cows to Dietary L-Carnitine

In Experiment 1, in vitro degradation of L-carnitine was measured in ruminal fluid obtained either from a cow that was fed a 75% concentrate diet or from a cow fed a control (50% forage and 3% fat) diet. Carnitine degradation was greater in ruminal fluid from the cow fed the control diet than in ruminal fluid from the cow fed the 75% concentrate diet and was more rapid in ruminal fluid obtained after 2 wk of adaptation to dietary carnitine supplementation (7 g/d). In Experiment 2, 20 multiparous Holstein cows were used in a replicated 5 × 5 Latin square design to determine the effects of increasing the amount of dietary L-carnitine (0, 0.875, 1.75, 3.5, or 7.0 g/d) that was fed to lactating dairy cows. All cows received the same diet, which contained 3% added fat.Carnitine concentration in milk and plasma increased linearly with carnitine supplementation. The DMI, milk yield, and milk composition were unaffected by carnitine. Apparent total tract digestibilities of NDF and fatty acids decreased quadratically as the amount of supplemented carnitine increased; generally, means were lowest when cows were fed 1.75 g/d of carnitine. The concentration of total VFA and molar percentages of individual VFA in ruminal fluid were unaffected by the amount of carnitine fed. Concentrations of glucose, NEFA, and urea N in plasma were unaffected by the amount of dietary carnitine; however, plasma cholesterol concentration decreased linearly as carnitine increased. Supplementation of ≤7.0 g/d of dietary carnitine did not benefit DMI, milk yield, milk composition, or digestive measurements in this experiment.

Renal adaptation to dietary carnitine in humans

Carnitine homeostasis in humans is maintained by dietary carnitine intake, a modest rate of endogenous carnitine synthesis, and efficient conservation of carnitine by the kidney. To assess the effect of dietary carnitine on the efficiency of carnitine reabsorption in humans, rates of carnitine excretion and reabsorption, indexed to the glomerular filtration rate, were determined over a range of plasma free and total carnitine concentrations in 12 strict vegetarians before and after dietary carnitine supplementation (0.248 mmol/d). This amount of dietary carnitine supplementation did not significantly increase plasma carnitine concentration and did not alter the glomerular filtration rate. At normal physiological plasma carnitine concentrations, the rate of carnitine excretion was increased and the rate of carnitine reabsorption was decreased by carnitine supplementation. We conclude that the kidney adapts to carnitine intake by reducing the efficiency of carnitine reabsorption.