ResearchPDF Available

L-carnitine in petfood

Authors:

Abstract

Some dog and cat foods contain L-carnitine added as a chemically pure substance. It generally concerns light foods, but also certain senior foods. The food packaging declares L-carnitine in the ingredient list and often says that it helps to burn fat and supports lean muscle mass. Or rather, it favors fat loss and muscle deposition, thus promoting a healthier body weight (1, 2). Along with light foods, veterinary weight-reduction, heart and liver diets may have added L-carnitine. L-carnitine is a vitamin-like compound that assists in delivering dietary and body fat to the energy-producing machinery of body cells. The L prefix refers to the active structure that is made in the body of dogs and cats, normally making carnitine supplementation unnecessary (3). Unsupplemented petfood provides L-carnitine through various ingredients, particularly those of animal origin. Supplemental L-carnitine is derived from bacterial or chemical synthesis, the latter process yielding 50% active and 50% inactive carnitine. Evidence suggests that supplemental L-carnitine stimulates fat burning in dogs and cats, which theoretically sets metabolism toward less body fat and more muscle amount. However, studies showed no L-carnitine effect on body-fat and non-fat amounts in cats, and negligible effects in dogs (Note 1). This holds for both weight-control and weight-reduction feeding regimens. In addition to its meaningless impact on body composition, there is no convincing proof that supplemental L-carnitine further enhances the rate of bodyweight loss during calorie-restricted feeding of dogs and cats. In free-feeding animals, L-carnitine did not reduce body weight. For weight maintenance and reduction, portion-controlled feeding of a nutritionally adequate food, with pet's body condition as compass, is still indicated.
Creature Companion 2018; August: 40, 42.
Anton C. Beynen
L-carnitine in petfood
Some dog and cat foods contain L-carnitine added as a chemically pure substance. It generally
concerns light foods, but also certain senior foods. The food packaging declares L-carnitine in the
ingredient list and often says that it helps to burn fat and supports lean muscle mass. Or rather, it
favors fat loss and muscle deposition, thus promoting a healthier body weight (1, 2). Along with
light foods, veterinary weight-reduction, heart and liver diets may have added L-carnitine.
L-carnitine is a vitamin-like compound that assists in delivering dietary and body fat to the energy-
producing machinery of body cells. The L prefix refers to the active structure that is made in the
body of dogs and cats, normally making carnitine supplementation unnecessary (3).
Unsupplemented petfood provides L-carnitine through various ingredients, particularly those of
animal origin. Supplemental L-carnitine is derived from bacterial or chemical synthesis, the latter
process yielding 50% active and 50% inactive carnitine.
Evidence suggests that supplemental L-carnitine stimulates fat burning in dogs and cats, which
theoretically sets metabolism toward less body fat and more muscle amount. However, studies
showed no L-carnitine effect on body-fat and non-fat amounts in cats, and negligible effects in
dogs (Note 1). This holds for both weight-control and weight-reduction feeding regimens.
In addition to its meaningless impact on body composition, there is no convincing proof that
supplemental L-carnitine further enhances the rate of body-weight loss during calorie-restricted
feeding of dogs and cats. In free-feeding animals, L-carnitine did not reduce body weight. For
weight maintenance and reduction, portion-controlled feeding of a nutritionally adequate food,
with pet’s body condition as compass, is still indicated.
L-carnitine
L-carnitine (4-tri-methylamino-3-hydroxybutyrate) and two carnitine palmitoyltransferases (CPTs)
carry fatty acyl groups from the cytosol into the cellular mitochondria. The acyls are oxidized into
acetyl-CoA that enters the tricarboxylic cycle and generates reducing equivalents for ATP synthesis.
Feeding extra L-carnitine, as beef or pure substance, raises plasma carnitine in dogs and cats (4-9). In
foxes fed animal byproducts, apparent ileal absorption of L-carnitine was 78% (10), but oral
supplements are much less available (11). Non-absorbed carnitine is degraded by colonic bacteria
(11).
Regular dry and wet petfoods contain 5 to 39 and 23 to 1450 mg L-carnitine/kg dietary dry matter
(ddm) (5, 6, 12-17, Note 2). Supplementation typically equals 50 to 350 mg/kg ddm, but is greater for
cardiac diets. An 11-kg dog consuming 200 g unsupplemented dry food/day may ingest 4 mg L-
carnitine/day while its biosynthesis (from lysine) equals 14 mg/day (12, 14, Note 3). L-carnitine is not
catabolized by dogs (12, 18) so that urinary excretion reflects absorption plus synthesis. At constant
L-carnitine intake, higher fat intake raised urinary loss in dogs (14).
Fatty acid oxidation
High-dose oral L-carnitine raised myocardial content in two carnitine-deficient dogs (4). L-carnitine
stimulated fatty acid oxidation in isolated dog cardiac myocytes (19) and skeletal muscle
homogenates (20). However, L-carnitine tissue concentrations and CPT-Km values (12, 21-23, Note 4)
indicate that supplemental dietary L-carnitine most likely stimulates hepatic fatty oxidation.
Adding L-carnitine to the diet lowered fasting plasma free fatty acids in cats (8) and dogs (9). In
restricted-fed, overweight cats, supplemental L-carnitine (76 vs 32 mg/kg ddm) lowered the
respiratory quotient, pointing at enhanced whole-body fatty acid oxidation (15), but corroboration is
meager (16).
Theoretical considerations
Percentages of the fat and fat-free masses in the body add up to 100%. In adult, normal-weight cats
and dogs, the distributions are about 30:70 and 20:80 (24). Can supplemental L-carnitine
theoretically lower body fat and consequently raise muscle mass (Note 5)?
L-carnitine may increase hepatic oxidation of fasting plasma fatty acids originating from adipose
tissue. Hepatic triacylglycerol secretion falls, but increased ATP production spares glucose, leading to
less gluconeogenesis, which in turn depresses muscle protein catabolism. Body fat shrinks due to
increased fatty acid release, but then stabilizes as more glucose is converted into fatty acids. Muscle
mass grows due to decreased protein catabolism, but then stabilizes while reinstating its catabolic
rate. At negative energy balance, L-carnitine may accelerate body-fat loss, thus conserving the fat-
free mass.
Body composition
Restricted-fed, overweight cats received diets containing 32 to 176 mg L-carnitine/kg ddm, but
baseline percentage body fat (%BF) was different for the low-dose group and not affected dose-
dependently in the other three groups (15). In a similar trial, supplemental L-carnitine (220 mg/kg
ddm) left %BF unchanged (25). In cats fed ad libitum, extra L-carnitine (500 mg/kg ddm) did not
influence %BF (26, Note 6).
In obese dogs with effective weight loss, L-carnitine lowered body fat, but effect size is unreported
(27). In dogs fed ad libitum for 7 weeks, L-carnitine (81 or 140 vs 24 mg/kg ddm) reduced %BF by 1
unit (13, 28, Note 7). During the following 12-weeks period of caloric restriction, L-carnitine-induced
lowering was 2 %units (13, 29, Note 7). In dogs fed to prevent weight gain, extra L-carnitine (300
mg/kg ddm) lowered fat percentage by 3.4 units (30, Note 8). In growing dogs, L-carnitine hardly
affected %BF (31).
Weight loss
In energy-restricted, obese cats, supplemental L-carnitine was associated with greater caloric deficit
(7), promoted weight loss (25) or did not (15). In dogs, L-carnitine did not enhance weight loss when
cutting their calories (13, 27).
Hepatic and cardiac diets
L-carnitine inconsistently protected against feline hepatic lipidosis (8, 25, 32, Note 9).
Therapeutically used L-carnitine doses are not met by commercial canine cardiac diets (33).
Note 1
In two dog studies, supplemental L-carnitine lowered percentage body fat (%BF) by 0.95, 2.05 (13,
Note 7) and 3.39 units (30, Note 8), the average being 2.1 units. One point difference in body score
on a 1 to 9 scale corresponds with 5 units difference in %BF (24). Thus, L-carnitine lowered body
condition by less than 0.5 point. This change of magnitude may not meaningfully affect longevity
(24). It is noteworthy that the reported group-mean %BF values (13, 30, Notes 7 and 8) seem very
high and low (cf. 24) and may be considered unrepresentative. In one study (13), fat-mass loss
during L-carnitine treatment was associated with a decrease in fat-free mass, but in the other study
(30) with an increase.
Note 2
The dry basal diets in reference 17 were assumed to contain 14.9 and 19.3 ppm L-carnitine.
Note 3
a. L-carnitine synthesis assessed as difference between excretion and intake (12): Data are means for
6 dogs. Body weight = 11.7 kg. L-carnitine intake: 1.99 µmol/h; excretion (urine + feces) = 5.37
µmol/h. Synthesis (excretion – intake) = 3.38 µmol/h = 13.1 mg/day. The rate of synthesis may be
underestimated due to bacterial L-carnitine degradation in the intestinal tract.
b. L-carnitine synthesis assessed as urinary excretion at zero L-carnitine intake (14): Data are means
for 6 dogs per dietary group. Body weight = 10.9 kg. Dietary L-carnitine levels: 20 and 344 mg/kg
dietary dry matter (ddm). Urinary L-carnitine excretion: 11,383 and 52,627 nmol/kg body weight per
24 hours = 20.0 and 92.5 mg/day. It follows that synthesis (urinary excretion at zero intake) = 15.5
mg/day.
Note 4
Tissue L-carnitine concentrations and L-carnitine Km values for CPT
Ref
Tissue
Species
Conc
1
2
12
Skeletal muscle
Dog
4.65
,,
Heart
,,
1.36
,,
Liver
,,
0.23
21
Skeletal muscle
Dog
0.63
,,
Heart
,,
0.70
22
Skeletal muscle
Dog
3.51
0.54
,,
Liver
,,
0.36
0.53
23
Skeletal muscle
Cat
1.24
0.42
,,
Liver
,,
0.23
0.44
1 mmol/kg wet tissue. 2 mmol/L
Note 5
When considering a theoretical framework for supplemental L-carnitine increasing hepatic fatty acid
oxidation and thereby changing body composition in adult animals, one prerequisite may be that a
new steady state develops while zero energy balance and identical macronutrient intake are
maintained. Thus, unaltered energy balance and altered body composition should be reconcilable.
In the fasting state, supplemental L-carnitine may stimulate hepatic oxidation of plasma fatty acids
originating from adipose tissue, which impairs hepatic triacylglycerol secretion. Both increased
hepatic ATP production and decreased uptake of triacylglycerols by muscle should be compensated
for. Less hepatic oxidation of glucose could counterbalance both the extra ATP derived from fatty
acid oxidation and the lower availability of triacylglycerols to muscle. At the same time, more
glucose being used by muscle may inhibit both muscular protein catabolism and hepatic
gluconeogenesis.
Increased fatty acid release by adipose tissue diminishes its size. Decreased protein breakdown
enlarges muscle mass to a stable size. The greater mass implies more substrate for catabolism so
that the original catabolic rate may be restored, including whole-body nitrogen balance. The
shrinking of adipose tissue stops and a smaller, steady size may be adopted. At this stage, more
glucose should be converted into fatty acids. If the changes in inter-tissue relationships in
metabolism occur indeed and correspond quantitatively, then, at zero energy balance and
unchanged macronutrient intake, supplemental L-carnitine may induce a new steady state in which
the amount of body fat is smaller and that of protein is larger.
At negative energy balance during calorie-restricted feeding, L-carnitine-induced additional
breakdown of dietary and body fatty acids may reduce amino acid oxidation, thus sparing muscle
protein. Thus, both at zero and negative energy balance, supplemental L-carnitine can theoretically
affect body composition in that body fat diminishes and muscle mass expands. However, in reality
such an effect may still not occur or be too small to detect.
Note 6
Healthy, but previously obese cats (n = 14 or 16/group) were fed ad libitum on the same food
without or with 500 mg added L-carnitine per kg ddm (26). Body composition was measured by dual
X-ray absorptiometry. After six months, the mean changes in lean mass were +46.3 and +192.4 g for
the control and supplemented cats. For body-fat mass, the changes were -96.6 and -85.1 g. When
assuming an initial body weight of 4 kg and fat mass of 1.2 kg (30%), the final fat masses of the
control and test cats are 1103.4 and 1114.9 g. Treatment had no effect on food intake. At constant
body weight, L-carnitine would have changed body fat from 27.6 to 27.9%.
Note 7
The table shows the effect of dietary L-carnitine on %BF in adult, ovariohysterectomized female
Beagle dogs. The dogs were fed ad libitum for 7 weeks, followed by food restriction for 12 weeks
(13).The L-carnitine effects on %BF, corrected for the unsupplemented control, are about 1 and 2
units lowering for the periods of weeks 0-7 and 7-19.
L
-
carnitine,
mg/kg ddm
Week 0
Week 7
Week 19
Δ
Weeks 0
-
7
Δ
Weeks 7
-
19
BW,
kg
BF, %
BW,
kg
BF,%
BW,
kg
BF, %
BW,
kg
BF, %
BW,
kg
BF,%
24*
14.9
41.6
14.5
38.6
13.0
35.3
-
0.4
-
3.0
-
1.5
-
3.3
81
14.8
40.5
13.4
36.4
12.1
31.2
-
1.4
-
4.1
-
1.3
-
5.2
140
15.0
41.3
14.0
37.5
12.6
32.0
-
1.0
-
3.8
-
1.4
-
5.5
*Unsupplemented control diet. Means for 10 dogs/group. BW = body weight; BF = body fat.
Note 8
Healthy, but previously obese Beagle dogs (n = 16/group) were fed the same food without or with
300 mg added L-carnitine per kg ddm, but in quantities that prevented body-weight gain (30). Body
composition was measured by dual X-ray absorptiometry. After six months, the mean changes in
lean mass were -0.05 and +1.2 kg for the control and supplemented dogs. For body-fat mass, the
changes were -1.7 and -2.1 kg; for body weight they were -1.7 and -0.9 kg. The publication in
abstract form expresses the weights as grams, but this is most likely erroneous. When assuming an
initial body weight of 15 kg and fat mass of 3 kg (20%), the final body weights of the control and test
dogs were 13.3 and 14.1 kg, with fat-masses of 1.3 and 0.9 kg. Consequently, the final body-fat
amounts would be 9.8 and 6.4%, so that L-carnitine-induced lowering was 3.4 %units.
Note 9
L-carnitine administered to cats in negative energy balance lowered (8) or raised (25) plasma beta-
hydroxybutyrate concentrations. In another study, beta-hydroxybutyrate was generally below the
level of detection in both control and supplemented cats (7).
Literature
1. Tudor K. Fat loss supplements for pets.
https://www.petmd.com/blogs/thedailyvet/ktudor/2012/may/fat_loss_supplements_for_pets-
16267
2. Owens K. Healthy pets thrive on nutritional supplementation.
https://totalhealthmagazine.com/Pet-Health/Healthy-Pets-Thrive-on-Nutritional-
Supplementation.html
3. National Research Council. Nutrient requirements of dogs and cats. The National Academies Press.
Washington, DC, 2006.
4. Keene BW, Panciera DP, Atkins CE, Regitz V, Schmidt MJ, Shug AL. Myocardial L-carnitine
deficiency in a family of dogs with dilated cardiomyopathy. J Am Vet Med Assoc 1991; 198: 647-650.
5. Shug AL, Keene BW. Method for preventing diet induced carnitine deficiency in domesticated dog
and cats. United States Patent number 4,883,672, Nov 28, 1998.
6. Iben Ch. Effects of L-carnitine administration on treadmill test performance of untrained dogs. J
Anim Physiol Anim Nutr 1999; 82: 66-79.
7. Center SA, Harte J, Watrous D, Reynolds A, Watson TDG, Markwell PJ, Millington DS, Wood PA,
Yeager AE, Erb HN. The clinical and metabolic effects of rapid weight loss in obese pet cats and the
influence of supplemental oral L-carnitine. J Vet Intern Med 2000; 14: 598-608.
8. Blanchard G, Paragon BM, Milliat F, Lutton C. Dietary L-carnitine supplementation in obese cats
alters carnitine metabolism and decreases ketosis during fasting and induced hepatic lipidosis. J Nutr
2002; 132: 204-210.
9. Epp TS, Erickson HH, Woodworth J, Poole DC. Effects of oral L-carnitine supplementation in racing
Greyhounds. Equine Comp Exerc Physiol 2008; 4: 141-147.
10. Szymeczko R, Burlikowska K, Iben C, Piotrowska A, Bogusławska-Tryk M. Ileal absorption of L-
carnitine from diets used in reproductive polar fox (Alopex lagopus L.) nutrition. Acta Agriculturae
Scand Section A 2007; 57: 142-147.
11. Rebouche CJ. Kinetics, pharmacokinetics, and regulation of L-carnitine and acetyl-L-carnitine
metabolism. Ann N Y Acad Sci 2004; 1033: 30-41.
12. Rebouche CJ, Engel AG. Kinetic compartmental analysis of carnitine metabolism in the dog. Arch
Biochem Biophys 1983; 220: 60-70.
13. Sunvold GD, Tetrick MA, Davenport GM. Process for promoting weight loss in overweight dogs.
United States Patent No 6,204,291 B1, Mar 20, 2001.
14. Sanderson SL, Osborne CA, Lulich JP, Gross KL, Lowry SR, Pierpont ME, Ogburn PN, Koehler LA,
Swanson LL, Bird KA, Ulrich LK. Effects of dietary fat and carnitine on urine carnitine excretion in
dogs. Vet Ther 2001; 2: 181-192.
15. Center SA, Warner KL, Randolph JF, Sunvold GD, Vickers JR. Influence of dietary supplementation
with L-carnitine on metabolic rate, fatty acid oxidation, body condition, and weight loss in
overweight cats. Am J Vet Res 2012; 73: 1002-1015.
16. Shoveller AK, Minikhiem DL, Carnagey K, Brewer J, Westendorf R, DiGennaro J, Gooding MA. Low
level of supplemental dietary L-carnitine increases energy expenditure in overweight, but not lean,
cats fed a moderate energy density diet to maintain body weight. Intern J Appl Res Vet Med 2014;
12: 33-43.
17. Varney JL, Fowler JW, Gilbert WC, Coon CN. Utilisation of supplemented L-carnitine for fuel
efficiency, as an antioxidant, and for mucle recovery in Labrador retrievers. J Nutr Sci 2017; 6: e8.
18. Yue KTN, Fritz IB. Fate of tritium-labeled carnitine administered to dogs and cats. Am J Physiol
1962; 202: 122-128.
19. Liu M-W, Spitzer JJ. Oxidation of palmitate and lactate by beating myocytes isolated from adult
dog heart. J Mol Cellular Cardiol 1978; 10: 415-426.
20. Long CS, Haller RG, Foster DW, McGarry JD. Kinetics of carnitine-dependent fatty acid oxidation.
Implications for human carnitine defiency. Neurology 1982; 32: 663-666.
21. McGarry JD, Mills SE, Long CS, Foster DW. Observations on the affinity for carnitine, and malonyl-
CoA sensitivity, of carnitine palmitoyltransferase I in animal and human tissues. Demonstration of
the presence of malonyl-CoA in non-hepatic tissues of the rat. Biochem J 1983; 214: 21-28.
22. Lin X, Odle J. Changes in kinetics of carnitine palmitoyltransferase in liver and skeletal muscle of
dogs (Canis familiaris) throughout growth and development. J Nutr 2003; 133: 1113-1119.
23. Lin X, House R, Odle J. Ontogeny and kinetics of carnitine palmitoyltransferase in liver and
skeletal muscle of the domestic felid (Felis domestica). J Nutr Biochem 2005; 16: 331-338.
24. Laflamme DP. Understanding and managing obesity in dogs and cats. Vet Clin Small Anim 2006;
36: 1283-1295.
25. Ibrahim WH, Bailey N, Sunvold GD, Bruckner GG. Effects of carnitine and taurine on fatty acid
metabolism and lipid accumulation in the liver of cats during weight gain and weight loss. Am J Vet
Res 2003; 64: 1265-1277.
26. Jewell DE, Toll PW. The effect of carnitine supplementation on body composition of obese-prone
cats. In: Obesity: weight management in cats and dogs. Hill’s Pet Nutrition, Topeka, KS, 1999, p 29.
27. Gross KL, Wedekind KJ, Kirk CA, Jewell DE. Effect of dietary carnitine or chromium on weight loss
and body composition of obese dogs. J Anim Sci 1998; 76 (Suppl 1): 175.
28. Sunvold GD, Tetrick MA, Davenport GM, Bouchard GF. Carnitine supplementation promotes
weight loss and decreased adiposity in the canine. Proceedings of the XXIII World Small Animal
Veterinary Association, 1998, p 746.
29. Sunvold GD, Vickers RJ, Kelley RL, Tetrick MA, Davenport GM, Bouchard GF. Effect of dietary
carnitine during energy restriction in the canine. FASEB J 1999; 13: A268.
30. Allen TA, Jewell DE, Toll PW. The effect of carnitine supplementation on body composition of
obese-prone dogs. In: Obesity: weight management in cats and dogs. Hill’s Pet Nutrition, Topeka, KS,
1999, p 27.
31. Gross KL, Zicker SC. L-carnitine increases muscle mass, bone mass and bone density in growing
large breed puppies. J Anim Sci 2000; 78 (Suppl 1): 176.
32. Armstrong PJ, Hardie EM, Cullen JM, Keene BW, Hand MS, Babineau CA. L-carnitine reduces
hepatic fat accumulation during rapid weight reduction in cats. J Vet Intern Med 1992; 6: 127.
33. Beynen AC. Canine cardiac diets: efficacy unproven. Dier-en-Arts 2017; Nr 1/2: 18-21.
DOI: 10.13140/RG.2.2.23978.11203
... Two spaniels with DCM were unresponsive to taurine supplementation, but in two others the combination of taurine and L-carnitine was effective (24). Possibly, the administration of L-carnitine stimulates fatty acid oxidation and energy production (25), and thereby myocardial contraction. American Cocker Spaniels (n= 5 or 6/group), with DCM and low plasma taurine received orally, three times a day, a placebo or taurine plus L-carnitine (26). ...
Article
Full-text available
Diet and taurine in canine cardiomyopathy* *Elaboration of article in Dutch (1) Main points Eleven days after the appearance of the Dutch version (1) of this write-up, the commentary of Freeman et al. (2) was published under the title "Diet-associated dilated cardiomyopathy in dogs: what do we know? The authors make a distinction between three groups of dogs with dilated cardiomyopathy (DCM): dogs with DCM completely unrelated to diet and dogs having diet-associated DCM with or without taurine deficiency (2). This paper focuses on DCM in dogs with diet-related taurine deficiency. Taurine deficiency is seen as potential cause of the canine cases of DCM in the US (3, 4). On July 12, 2018, the FDA (Food and Drug Administration) made an announcement about arrived reports on DCM in dogs (5). Numbers and arrival dates of the reports were not disclosed. The FDA mentioned that, according to the ingredient lists, the foods fed to the sick dogs were rich in peas, lentils, other legume seeds or potatoes. Because the FDA loosely typified the dogs' foods as grain-free (5), its announcement sometimes has been passed on as an association between grain-free food and DCM (4, 6). Based on their own experience, Freeman et al. (2) feel that diet-associated DCM is not necessarily tied to the grain-free status of the diet. It is currently unknown whether or not the diet plays a role in the DCM cases (2). Causality is illogical given the variation within the foods supplied to the affected dogs. A diet effect would be plausible when one ingredient (from the same supplier) or one or more food brands (from the same manufacturer) is the common factor of the cases. Taurine deficiency is not evident. First, most dogs with DCM do not have low plasma taurine (7). Secondly, the FDA noted that whole blood taurine, which was analysed in 8 DCM patients, was either low or normal in half of them (5). The suggestion that diet-induced taurine deficiency underlies the US outbreak of canine DCM (3, 4) reminds of observations published in 2003 (8). Twelve dogs of different breeds shared DCM, low plasma taurine and specific lamb-meal containing foods. Understandably, no attempts have been made to induce DCM in dogs by feeding them a suspect lamb-meal diet. The effects on taurine metabolism of doubtful lamb meal preparations as only dietary variable have not been studied. Results of the follow-up studies (8-11) point to an unfortunate coincidence as explanation for the DCM cases: a diet-induced, additional lowering of individually-determined, undersized taurine synthesis. This communication elaborates on the possible metabolic basis of taurine deficiency in diet-associated canine DCM. Taurine The chemical name of taurine is 2-aminoethanesulfonic acid. Taurine does not have a carboxyl group, is not an alpha-amino acid, and thus cannot be an intra-molecular part of proteins. It is mainly present in the cytosol of animal cells, particularly organ cells. Shellfish has high taurine contents.
Research
Full-text available
Canine cardiac diets: efficacy unproven
Article
Full-text available
The primary goal was to investigate the effects of l -carnitine on fuel efficiency, as an antioxidant, and for muscle recovery in Labrador retrievers. Dogs were split into two groups, with one group being supplemented with 250 mg/d of Carniking™ l -carnitine powder. Two experiments (Expt 1 and Expt 2) were performed over a 2-year period which included running programmes, activity monitoring, body composition scans and evaluation of recovery using biomarkers. Each experiment differed slightly in dog number and design: fifty-six v . forty dogs; one endurance and two sprint runs per week v . two endurance runs; and differing blood collection time points. All dogs were fed a low-carnitine diet in which a fixed amount was offered based on maintaining the minimum starting weight. Results from Expt 1 found that the carnitine dogs produced approximately 4000 more activity points per km compared with the control group during sprint ( P = 0·052) and endurance runs ( P = 0·0001). Male carnitine dogs produced half the creatine phosphokinase (CPK) following exercise compared with male control dogs ( P = 0·05). Carnitine dogs had lower myoglobin at 6·69 ng/ml following intensive exercise compared with controls at 24·02 ng/ml ( P = 0·0295). Total antioxidant capacity (TAC) and thiobarbituric acid reactive substance (TBARS) results were not considered significant. In Expt 2, body composition scans indicated that the carnitine group gained more total tissue mass while controls lost tissue mass ( P = 0·0006) and also gained lean mass while the control group lost lean mass ( P < 0·0001). Carnitine dogs had lower CPK secretion at 23·06 v . control at 28·37 mU/ml 24 h after post-run ( P = 0·003). Myoglobin levels were lower in carnitine v . control dogs both 1 h post-run ( P = 0·0157; 23·83 v . 37·91 ng/ml) and 24 h post-run ( P = 0·0189; 6·25 v .13·5 ng/ml). TAC indicated more antioxidant activity in carnitine dogs at 0·16 m mv . control at 0·13 m m ( P = 0·0496). TBARS were also significantly lower in carnitine dogs both pre-run ( P = 0·0013; 15·36 v . 23·42 µ m ) and 1 h post-run ( P = 0·056; 16·45 v . 20·65 µ m ). Supplementing l -carnitine in the form of Carniking™ had positive benefits in Labrador retrievers for activity intensity, body composition, muscle recovery and oxidative capacity.
Article
Full-text available
Five mature ileorectal anastomosed blue foxes (6.18±0.15 kg) were used in digestibility experiments to evaluate the L-carnitine apparent ileal absorption from diets used in reproductive polar fox nutrition over the year-long farm-feeding period on two domestic farms (A and B) differing in reproduction results. The concentration of L-carnitine was higher in diets from farm B (136.1–241.7 mg kg DM) than in the diets from farm A (88.5–135.2 mg kg DM). The coefficients of ileal apparent absorption of L-carnitine ranged from 60.23 to 75.57% for diets A (farm A) composed mainly of fish and poultry offals. The coefficients of ileal apparent digestibility of L-carnitine were higher for diets B (farm B) (83.75–94.78%; P
Article
L-carnitine (LC) has been included in feline diets to enhance weight loss and reduce risk of hepatic lipidosis. However, many overweight cats are fed maintenance diets and are not undergoing weight loss. The objective of this study was to investigate how feeding lean and overweight adult cats dietary LC (100 mg/kg) during weight maintenance affected resting energy expenditure (EE), respiratory quotient (RQ), and play motivation. Twenty healthy adult cats were stratified by gender and body condition score (BCS) and randomly assigned to receive either a control food (CON) or the same food supplemented with 100 mg/ kg LC (LC+) for 42 days. EE was assessed using indirect calorimetry at 0, 21, and 42 days and play motivation was assessed at 0 and 42 days. Body weight did not differ between treatment groups at baseline and throughout the study (P>0.05), as expected. On days 21 and 42, area under the curve (AUC) for EE (kcal/ kg BW*d) and RQ did not differ between groups (P>0.05) for lean cats. However, overweight cats fed LC+ had greater (P<0.05) AUC for EE for at fasting and after receiving a meal on d 21 and 42 and a lower AUC for RQ from 0 - 210 minutes post feeding on d 42 than overweight cats fed CON. Overweight cats, but not lean cats, fed LC+ spent less time both in the start box and overall test and pushed more weight in the obstruction test than cats fed CON (P<0.05). These results suggest that dietary LC fed at a low level of supplementation results in greater EE, lower RQ, and greater motivation to play in overweight, but not lean, cats fed to maintain weight. Future research should investigate whether a similar mechanism is present in cats fed ad libitum, the feeding management strategy commonly used.
l-Carnitine supplementation can stimulate erythropoiesis, reduce exercise-induced plasma lactate concentrations and decrease post-exercise muscle damage. Next to horses, Greyhounds represent the premier animal racing species and perform short-duration, very high-intensity exercise that has the potential to incur substantial muscle damage. Under resting and standard racing conditions (5/16 mile), we tested the novel hypotheses that l-carnitine supplementation in Greyhounds would: (1) elevate haematocrit at rest and immediately post-exercise; (2) reduce peak post-exercise plasma lactate; and (3) reduce indices of muscle damage (plasma creatine phosphokinase, CPK and aspartate aminotransferase, AST). Six conditioned Greyhounds (30.1 ± 1.6 kg) underwent a randomized placebo-controlled crossover study to determine the effects of 6 weeks of l-carnitine supplementation (100 mg kg− 1 of body weight/day) at rest and following a maximal speed 5/16 mile race. In accordance with our hypotheses, l-carnitine elevated resting and immediately post-race haematocrit (control, 60.1 ± 1.7, l-carnitine, 63.6 ± 1.7; P < 0.05) and reduced peak post-race plasma CPK and AST concentrations (both P < 0.05). Those dogs with the highest peak post-exercise plasma CPK concentrations under placebo conditions evidenced the greatest reduction with l-carnitine supplementation (r = 0.99, P < 0.01). However, contrary to our hypotheses, l-carnitine did not change peak post-exercise plasma lactate concentrations (control, 27.0 ± 2.1, l-carnitine, 27.7 ± 1.3; P>0.05). We conclude that l-carnitine supplementation increases the potential for oxygen transport and reduces plasma indicators of muscle damage, CPK and AST in racing Greyhounds.
Article
Introduction Carnitine (trimethyl-γ-amino-β-hydroxybutyrate; molecular weight 161 g) is not only essential for the transport and utilization of long-chain fatty acids, it also occurs as a medium and short-chain ester and serves as an acetyl and acyl pool. Short-term muscle exercise causes an increase of acetyl-carnitine levels in the serum and in the liver. It prevents the accumulation of acyl-coenzyme A (CoA) and provides the organism with CoA by producing acetyl-carnitine from acetyl-CoA. Human muscle tissue contains approximately 10 μmol CoA/kg, whereas carnitine levels range between 2000 and 5000 μmol/kg.
Article
To investigate the influence of dietary supplementation with l-carnitine on metabolic rate, fatty acid oxidation, weight loss, and lean body mass (LBM) in overweight cats undergoing rapid weight reduction. 32 healthy adult neutered colony-housed cats. Cats fattened through unrestricted ingestion of an energy-dense diet for 6 months were randomly assigned to 4 groups and fed a weight reduction diet supplemented with 0 (control), 50, 100, or 150 μg of carnitine/g of diet (unrestricted for 1 month, then restricted). Measurements included resting energy expenditure, respiratory quotient, daily energy expenditure, LBM, and fatty acid oxidation. Following weight loss, cats were allowed unrestricted feeding of the energy-dense diet to investigate weight gain after test diet cessation. Median weekly weight loss in all groups was ≥ 1.3%, with no difference among groups in overall or cumulative percentage weight loss. During restricted feeding, the resting energy expenditure-to-LBM ratio was significantly higher in cats that received l-carnitine than in those that received the control diet. Respiratory quotient was significantly lower in each cat that received l-carnitine on day 42, compared with the value before the diet began, and in all cats that received l-carnitine, compared with the control group throughout restricted feeding. A significant increase in palmitate flux rate in cats fed the diet with 150 μg of carnitine/g relative to the flux rate in the control group on day 42 corresponded to significantly increased stoichiometric fat oxidation in the l-carnitine diet group (> 62% vs 14% for the control group). Weight gain (as high as 28%) was evident within 35 days after unrestricted feeding was reintroduced. Dietary l-carnitine supplementation appeared to have a metabolic effect in overweight cats undergoing rapid weight loss that facilitated fatty acid oxidation.
Article
This study was undertaken to quantitate the dynamic parameters of carnitine metabolism in the dog. Six mongrel dogs were given intravenous injections of l-[methyl-3H]carnitine and the specific radioactivity of carnitine was followed in plasma and urine for 19–28 days. The data were analyzed by kinetic compartmental analysis. A three-compartment, open-system model [(a) extracellular fluid, (b) cardiac and skeletal muscle, (c) other tissues, particularly liver and kidney] was adopted and kinetic parameters (carnitine flux, pool sizes, kinetic constants) were derived. In four of six dogs the size of the muscle carnitine pool obtained by kinetic compartmental analysis agreed (±5%) with estimates based on measurement of carnitine concentrations in different muscles. In three of six dogs carnitine excretion rates derived from kinetic compartmental analysis agreed (±9%) with experimentally measured values, but in three dogs the rates by kinetic compartmental analysis were significantly higher than the corresponding rates measured directly. Appropriate chromatographic analyses revealed no radioactive metabolites in muscle or urine of any of the dogs. Turnover times for carnitine were (mean ± SEM): 0.44 ± 0.05 h for extracellular fluid, 232 ± 22 h for muscle, and 7.9 ± 1.1 h for other tissues. The estimated flux of carnitine in muscle was 210 pmol/min/g of tissue. Whole-body turnover time for carnitine was 62.9 ± 5.6 days (mean ± SEM). Estimated carnitine biosynthesis ranged from 2.9 to 28 μmol/kg body wt/day. Results of this study indicate that kinetic compartmental analysis may be applicable to study of human carnitine metabolism.
Article
Myocytes were isolated from hearts of adult dogs by repeated digestion with collagenase and hyaluronidase in Ca2+-free phosphate buffer followed by centrifugation in the presence of Ficoll. The isolated myocytes were free of other tissue elements and were contracting autorhythmically. The oxidation of palmitate and lactate were studied by incubating cell preparation with [1-14C]palmitate or [U-14C]lactate either in the presence or absence of CaCl2 for 30 min at 37°C. [14C]O2 was collected by KOH-soaked filter paper. Cardiac myocytes oxidized 0.1 to 0.18 nmol/mg protein min of palmitate and 1.5 to 2.2 nmol/mg protein min of lactate. The oxidation was linear for 75 min. Maximal rate of oxidation was obtained at substrate concentrations of 0.2 mm palmitate or 5.0 mm lactate. Adenine or pyridine nucleotides had no effect on the oxidation of these substrates. Palmitate oxidation was enhanced by carnitine and also by an increase in the molar ratio of palmitate/albumin, but was depressed (15 to 50%) by CaCl2 (0.025 to 1.0 mm). CaCl2 (0.05 to 1.0 mm) increased the rate of lactate oxidation by 50 to 68%. Lactate oxidation was also enhanced (68 to 87%) in the presence of palmitate (0.4 to 0.8 mm). These findings demonstrate the suitability of isolated adult heart myocytes for the study of cardiac metabolism.
Article
Turnover of carnitine in the body is primarily the result of renal excretion, and high-fat (HF) diets have been shown to increase urine carnitine excretion in healthy people. Recently, increased renal excretion of carnitine was observed in dogs diagnosed with cystinuria and carnitine deficiency. Carnitine deficiency has been linked to dilated cardiomyopathy and lipid storage myopathies in dogs and humans, and low-fat (LF) diets have been beneficial in some human patients with carnitine deficiency. In addition, HF, protein-restricted diets are often recommended for management of cystinuria in dogs. However, whether HF diets increase renal carnitine excretion in dogs or whether dogs with carnitine deficiency would benefit from LF diets remains unknown. Therefore, the purpose of this study was to determine the influence of dietary fat and carnitine on renal carnitine excretion in healthy dogs. Results from this study revealed that an HF diet increased urine carnitine excretion in dogs; however, carnitine excretion with the HF diet was not significantly different from that in dogs consuming an LF diet. Nonetheless, these results raise the possibility that increased renal carnitine excretion associated with HF diets could be one risk factor for development of carnitine deficiency in dogs with an underlying disorder in carnitine metabolism, and some dogs with carnitine deficiency may benefit from an LF diet. Another important observation in this study was that renal excretion of carnitine exceeded dietary intake in all diet groups, confirming previous reports that concluded that canine renal tubular cells reabsorb carnitine poorly when compared with those of humans.