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 (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
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
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-
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).
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).
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.
The dry basal diets in reference 17 were assumed to contain 14.9 and 19.3 ppm L-carnitine.
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
Tissue L-carnitine concentrations and L-carnitine Km values for CPT
1 mmol/kg wet tissue. 2 mmol/L
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
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.
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%.
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.
*Unsupplemented control diet. Means for 10 dogs/group. BW = body weight; BF = body fat.
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.
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).
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