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Department of Nutrition and Agricultural Experiment Station, The University of Tennessee, Knoxville, TN 37996-1900
3To whom correspondence should be addressed.
 |
ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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0.01), fat pad weight (r = 0.82, P 0.001) and serum glucose
(r = 0.51, P 0.05). We
conclude that the indices of body fat loss due to dietary supplements
were similar to those due to mild exercise, and there were no
interactive effects of the two variables.
KEY WORDS: • adiposity • choline • carnitine • caffeine • leptin • exercise • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Clinical studies have shown that carnitine
supplementation improves muscle function in patients with carnitine
deficiency (Brass and Hiatt 1994
). Several studies
suggest an increased carnitine utilization during endurance exercise in
humans (Decombaz et al. 1992
, Lennon et al. 1983
). However, there is no clear agreement on the benefits of
carnitine supplementation in normal healthy individuals (Neumann 1996
). Choline is a lipotropic agent (Best and Huntsman 1935
, Leiber et al. 1994
), and its
supplementation has been shown to enhance synthesis and release of
acetylcholine at the neuromuscular junction (Buyukuysal et al. 1995
, Zeisel and Blusztajn 1994
). It has been
observed that there is a decline in plasma choline concentration in
athletes after running a marathon (Conlay et al. 1992
).
Therefore, choline supplementation may improve acetylcholine balance
and prevent decrement in physical performance. However, there are no
definitive studies on the effects of choline supplementation in normal
healthy people. Caffeine is used widely as a general stimulant and a
fatty acid mobilizer from adipose tissues (Bellet et al. 1968
, Costill et al. 1978
, Denadai 1994
). It has been hypothesized that fat-mobilizing effects
of caffeine and other methylxanthines elevate blood free fatty acid
concentration and spare carbohydrate stores, prolonging endurance
exercise. However, this hypothesis remains controversial because of a
lack of standardized experimental procedures: the type, intensity and
duration of training, the dose of caffeine used and habitual use of
caffeine by participants (Nehlig and Debry 1994
).
Recently, we reported interactive effects of choline and carnitine in
normal healthy humans and animals. Choline supplementation resulted in
significant conservation of carnitine in humans and guinea pigs
(Daily and Sachan 1995
, Dodson and Sachan 1996
); however, this effect of choline was not seen in the
adult rats given choline dosage similar to that given to humans and
guinea pigs (Daily and Sachan 1995
, Rein et al. 1997
). The choline supplementation promoted tissue carnitine
accretion, particularly in skeletal muscle of guinea pigs (Daily and Sachan 1995
) and livers of rats (Rein et al. 1997
). In addition, a choline-supplemented diet decreased
percentage of body fat and increased percentage of protein without
significantly changing body weight or the respiratory exchange ratio in
guinea pigs (Daily et al. 1998
). Guinea pigs would have
been a preferred animal model for their likeness to humans with regard
to choline carnitine interactions, but guinea pigs are not easily made
to exercise on a treadmill. So, we settled on a rat as a model with
modification of dietary treatment in two ways. First, we increased the
supplementary level of choline to about fivefold used in guinea pigs or
humans. Second, we included caffeine as one of the supplements for its
fat-mobilizing property. We rationalized that besides increasing
energy demand by exercising muscle, simultaneous availability of
caffeine, carnitine and choline may induce mobilization, transport and
delivery of fat as the energy substrate of choice. This theoretically
sound rationale required experimental evidence which is presented in
this paper.
Leptin, a 16-kDa protein released from adipose tissue as a
product of the obese (ob) gene (Zhang et al. 1994
), is thought to play a role in the regulation of body
weight, energy expenditure and food intake (Campfield et al. 1995
, Halaas et al. 1995
, Pelleymounter et al. 1995
). Studies have shown that leptin circulates in
proportion to body fat mass in humans (Considine et al. 1996
) and rodents (Ahren et al. 1997
) and
reflects body lipid content in mice (Frederich et al. 1995
). The data on effects of nutritional perturbations on
serum leptin are beginning to accumulate. For example, serum leptin
concentration falls after fasting (Boden et al. 1996
)
and energy restriction (Wadden et al. 1998
) with
relatively small decreases in body weight and fat mass. In addition,
serum leptin concentrations fell following ultramarathon running in men
(Landt et al. 1997
) and 12 wk of aerobic exercise in
women without changes in adiposity (Hickey et al. 1997
).
The list of nutritional factors that influence circulating leptin
concentrations is small, and there are no studies on the effect of
dietary supplements plus exercise on circulating serum leptin
concentrations. Thus the objective of this study was to determine
changes in body weight, fat pad weights, serum leptin concentrations
and metabolic indices in rats fed a diet supplemented with caffeine,
carnitine and choline with and without exercise.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The protocol of this study was approved by the University of Tennessee Institutional Review Board. Twenty, 7-wk-old male Sprague-Dawley rats (Harlan Sprague-Dawley, Indianapolis, IN) were housed in a room controlled for temperature (20–22°C), relative humidity (50%), and light (12-h light/dark cycle). Their initial mean body weight was 218 g. Rats had free access to a ground nonpurified diet, Harlan Teklad 22/5; protein 22%, fat 5% and fiber 3.83%, (Harlan Teklad, Madison, WI) and water. The diet was fortified with caffeine, carnitine and choline at concentrations of 0.1, 5 and 11.5 g/kg nonpurified diet, respectively, as the supplemented diet.
The endogenous concentrations of choline and carnitine in this commercial diet were 2.1 g and 30 mg/kg diet, respectively. All rats were weighed daily, and their food intake was determined daily by the difference in the weight of food containers. Daily food intakes throughout the 4-wk experimental period were used to calculate average food intake. After arrival (1 wk), the rats were randomly divided into two groups (n = 10) and assigned to the nonsupplemented or supplemented diet. Each dietary group was subdivided into exercised and nonexercised groups (n = 5).
One-half of each dietary group was exercised on a rodent treadmill (Columbus Instruments International, Columbus, OH). All rats in exercise groups were made to run on the treadmill for 10 min at 15% grade starting at wk 3. The running speed and duration were continuously increased during the course of exercise to maximize at 18 m/min for 25 min/d. The 2 x 2 factorial design was scheduled as follows: wk 1, all rats consumed the nonsupplemented diet; wk 2, one-half of the rats consumed the nonsupplemented diet and one-half did the supplemented diet; wk 3, one-half of the nonsupplemented and supplemented rats were made to exercise on a treadmill 5 d/wk; wk 4, the diet and exercise regimen continued; and wk 5, the same treatments as in wk 4.
Sample collection and assays.
At the end of the 5-wk experimental period, rats were anesthetized with
methoxyflurane (Pitman-Moore, Mundelein, IL) and killed by
exsanguination after cardiocentesis using 10-mL syringes fitted with
23-gauge, 1.9-cm disposable needles. The blood samples were immediately
centrifuged at 2000 x g for 10 min at 4°C. Serum
was removed and stored at -80°C until used for determination of
glucose, triglycerides, free fatty acids and leptin concentrations.
Following blood collection, regional fat pads of epididymal, perirenal
and inguinal fat were quickly excised from the carcasses, weighed,
rinsed with saline, blotted dry, frozen in liquid nitrogen and stored
at -80°C until used for triglycerides and total lipid determination.
Glucose was determined by glucose oxidase method using Sigma kit no.
510 (Sigma, St. Louis, MO). Triglycerides, total lipid, nonesterified
fatty acids and lactate were determined by the methods of Giegel et al. (1975)
, Ellefson and Caraway (1976)
, Novak (1965)
and Gutmann and Wahlefeld (1974)
, respectively. Serum leptin concentrations were
determined using a commercial radioimmunoassay kit (Linco Research, St.
Louis, MO).
Statistical analysis.
All results are presented as group means ± SEM. Data
were analyzed using two-way ANOVA to test the effects of exercise,
supplementation and their interaction using SAS (1997)
. The main
effects of diet and exercise were tested using specific linear
contrasts, as was the interaction. Pearson correlation coefficients
were calculated using data from all 20 rats. Statistical significance
level was set at P 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Supplemented rats consumed in their diets ~2.1, 105 and 240 mg/d of
caffeine, carnitine and choline, respectively. The final body weight
and weight gain of the exercised rats were significantly lower
(P = 0.001) than those of nonexercised rats with or
without supplement (Table 1)
. There were no significant differences in
food intakes of the groups.
|
). The weights of the epididymal fat pad of exercised, supplemented rats
were significantly lower than their nonexercised counterparts. The
weights of inguinal fat pads of exercised rats with and without
supplementation were significantly lower than their paired nonexercised
rats. The weights of perirenal fat pads of exercised rats were
significantly lower than their nonexercised counterparts. The perirenal
fat pad weights of the supplemented, nonexercised rats were lower than
those of the nonexercised, nonsupplemented rats. Total fat pad weight
(sum of the three) showed a pattern similar to that of the other three
fat pads, particularly the inguinal fat pad weight. Although the
duration and intensity of exercise were the same in the two exercised
groups, total fat pad reductions due to exercise were 25% in
nonsupplemented rats and 44% in supplemented rats, compared to the
nonsupplemented, nonexercised rats. However, there was not a
significant interaction between diet and exercise.
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). The total lipid of epididymal and perirenal fat pads was
significantly lower in exercised, supplemented rats compared to
nonexercised controls, reflecting the difference in the corresponding
fat pad weight (Table 2)
. The effects of both supplement and exercise
on total lipid were remarkable in the inguinal fat pad as there was
62% less total lipid in the exercised, supplemented rats compared to
the nonsupplemented, nonexercised rats. However, the interactive
effects of supplement and exercise were not significant. The
triglycerides of epididymal fat pads were affected by exercise;
however, those of the inguinal and perirenal fat pads were not
significantly affected by either supplementation or exercise. The total
lipids made up ~80–90% of the fat pad weights, and 70–80% of the
total lipids were triglycerides.
|
). Serum leptin concentration was significantly lower in the exercised,
supplemented rats compared to any other group. Supplementation and
exercise did not significantly affect serum glucose, lactate or free
fatty acids.
|
). Serum leptin concentrations were correlated with serum glucose but
not with food intake.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Dodson and Sachan 1996
). This conservation
of carnitine in guinea pigs resulted in accretion of carnitine in all
tissues, especially skeletal muscle, where the differences were
significant (Daily and Sachan 1995
). The exercise
regimen is difficult to impose upon guinea pigs because they do not run
very well on a treadmill. Rats, on the other hand, will run on a
treadmill which enhances adipose tissue turnover rate (Askew et al. 1977
). However, rats do not conserve carnitine as do humans
or guinea pigs at an equivalent dosage of choline (Daily and Sachan 1995
). This was believed to be due to very high activity
of choline oxidase in rat liver compared to that in guinea pigs or
humans (Sidransky and Farber 1960
). We speculated that
high choline oxidase activity may be counterbalanced by high levels of
choline supplementation in the rat diet. Therefore, supplementary
choline level in the nonpurified diet was about fivefold endogenous
levels and that used in earlier rat studies by us (Daily and Sachan 1995
) and others (Rein et al. 1997
).
After taking into account the daily food consumption by the rats (Table 1)
, it is estimated that caffeine, carnitine and choline intakes were
6, 300 and 800 mg/kg of body weight. The pharmacological doses of
caffeine, carnitine and choline in humans are 7–14, 40–45 and
150–200 mg/kg body weight, respectively. Thus choline and carnitine
were four- to sixfold higher than usual dosage but far below the toxic
dosage (LD50 of choline in rat is 3.4–6.7 g/kg
body weight and none established for carnitine). It was anticipated
that this amount of choline may be more than sufficient to compensate
for the high activity of rat choline oxidase and therefore, may induce
significant carnitine conservation. Choline supplemented at 10 g/kg
diet (seven- to tenfold higher than normal) and fed for 1–42 d
increased urinary excretion of choline 19-fold in rats just after
1 d of feeding the diet (Rein et al. 1997
). In
guinea pigs, choline supplementation (3 g choline/kg diet) over and
above the normal dietary choline concentration (1.8 mg/kg), resulted in
eight- to ninefold higher choline excretion in the urine. These
observations indicate that supplementary choline must get into the
systemic circulation before it can be filtered into urine at these high
concentrations. We can only assume that enough choline escapes choline
oxidase to bring about the anticipated conservation of carnitine.
The combination of choline, carnitine and caffeine superimposed with
mild exercise was hypothesized to enhance oxidation of fat by skeletal
muscle and as a consequence reduce the amount of body fat. Mild
exercise preferentially promotes fat oxidation for meeting energy needs
over and above the basal energy requirements (Romijn et al. 1993
). The results of this study support this hypothesis as
there was significant loss of adipose fat mass in the supplemented as
well as exercised rats in 4 wk (Table 2)
. This is important because
carnitine alone had no significant effect on perirenal fat pad weight
of rats fed 0.5% carnitine-supplemented diet and trained on
treadmill for 5 wk (Askew et al. 1977
). Diets
supplemented with carnitine alone have produced variable responses
regarding substrate utilization and muscle fatigue in exercise
(Brass and Hiatt 1994
, Decombaz et al. 1992
, Lennon et al. 1983
, Neumann 1996
). Similarly, choline alone is not known to alter energy
substrate utilization (Spector et al. 1995
) or reduce
body weight (Tsai et al. 1974
). Likewise, caffeine alone
has been shown to increase plasma free fatty acid concentration without
altering substrate preference for oxidation in running exercise
(Casal and Leon 1985
). Caffeine by itself at a dosage of
200 mg, three times a day for 24 wk had no effect on body weight in
obese patients. However, when combined with 20 mg of ephedrine, it
caused a significant decrease in body weight (Astrup et al. 1992
).
The reduction in body fat is supported by reduction in the endogenous
marker of adiposity, leptin, which was significantly lower in the
supplemented as well as the exercised rats (Table 4)
. The leptin
concentrations were positively correlated with body fat (r
= 0.82, P < 0.001) and body weight (r
= 0.55, P < 0.01) as shown in Table 5
and has
been seen elsewhere (Ahren et al. 1997
, Frederich et al. 1995
). Factors other than adipose tissue mass influence
leptin secretion (Havel 1998
). For example, the decrease
in circulating leptin concentration during energy restriction in humans
is closely related to the decrease in plasma glucose (Dubuc et al. 1998
). However, in the rats of our study, feed-intake
was not affected by any of the treatments (Table 1)
, and serum
concentration of leptin was positively correlated with serum glucose
(r = 0.51, P < 0.05).
The differences in the concentrations of the metabolites presented in
Table 4
suggest that supplementation favored partitioning of
triglycerides from serum to skeletal muscle because there was a
33–46% lower concentration in serum and 82–90% greater level in the
muscle. Increased esterification and increased permeability of muscle
membranes to fatty acids are possible (Marconi et al. 1985
, Neumann 1996
). Lower concentrations of
serum glucose (13%) and free fatty acids (31%) in the supplemented,
exercised group also suggest a promotion of energy substrate
utilization by supplementation under the conditions of mild exercise.
Mild exercise has been shown to promote preferential use of fat for
energy needs over and above the basal requirements (Romijn et al. 1993
).
We thought it was relevant to characterize the chemical nature of the
adipose fat mass which was found to be 80–90% total lipids of which
70–80% were triglycerides (Table 3)
. These values are close to the
upper end of the range of lipid contents of adipose tissue. Adipose
tissue is, on the average, 80% fat, 18% water and 2% protein
(Heymsfield et al. 1999
). The protein contents of the
adipose tissues were not different among the groups (data not shown).
From these data, clearly, the combination of choline, carnitine and caffeine with or without mild exercise reduces body fat, as indicated by a decrease in fat pad weights and total lipids as well as serum leptin in rats. We conclude that the dietary supplement used in this study promotes fat loss as much as does the exercise, and there is no significant interactive effect. This does not preclude reassessment of individual effects of the components of this supplement. These results may or may not be applicable to humans, and further research is necessary to determine whether similar effects would result in other species.
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FOOTNOTES |
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2 Supported by the Agricultural Experiment Station of The University of Tennessee.
Manuscript received August 20, 1999. Initial review completed September 27, 1999. Revision accepted November 3, 1999.
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