Recent Advances in Nutritional Sciences Physiological Effects of Medium-
the liver for rapid oxidation (1). LCT, however, are transportedvia chylomicrons into the lymphatic system, allowing for exten-
Chain Triglycerides: Potential
sive uptake into adipose tissue. Therefore, it has been hypothe-
Agents in the Prevention
sized that the rapid metabolism of MCT may increase energyexpenditure (EE), decrease their deposition into adipose tissue
of Obesity1
and result in faster satiety. The objective of the present article isto review literature concerning the effects of MCT on EE, fat
Marie-Pierre St-Onge and Peter J. H. Jones2
deposition and food intake as a means to establish the potentialefficacy of MCT in the prevention of obesity in humans. School of Dietetics and Human Nutrition, McGill University,Ste-Anne-de-Bellevue, Quebec, Canada, H9X 3V9Effect of MCT on Energy Expenditure. Animal trials studying the effects of MCT vs. LCT consumption on lipid ABSTRACT Medium chain fatty acids (MCFA) are readily
and energy metabolism have shown that body weight (BW) is
oxidized in the liver. Animal and human studies have shown
reduced with MCT consumption compared with LCT con-
that the fast rate of oxidation of MCFA leads to greater
sumption and that feed efficiency is thus reduced (9 –11). In a
energy expenditure (EE). Most animal studies have also
study in which rats infused with MCT gained one third of the
demonstrated that the greater EE with MCFA relative to
weight gained by those infused with LCT, Lasekan et al. (9)
long-chain fatty acids (LCFA) results in less body weight
concluded that replacing LCT with MCT over long periods
gain and decreased size of fat depots after several months
could produce weight loss without decreasing energy intakes. of consumption. Furthermore, both animal and human trials
Human studies have mainly compared the effects of MCT
suggest a greater satiating effect of medium-chain triglyc-
vs. LCT in single-meal or single-day experiments. Scalfi et al. erides (MCT) compared with long-chain triglycerides (LCT).
(3) evaluated the effects of a single mixed meal containing
The aim of this review is to evaluate existing data describ-
MCT on postprandial thermogenesis and examined possible
ing the effects of MCT on EE and satiety and determine
differences in the thermic response between lean and obese
their potential efficacy as agents in the treatment of human
men. Subjects consumed a meal containing 15% of energy
obesity. Animal studies are summarized and human trials
from protein, 55% from carbohydrate and 30% from fat, in the
more systematically evaluated because the primary focus
form of corn oil (CO) and animal fat or MCT oil (56%
of this article is to examine the effects of MCT on human
octanoate, 40% decanoate) in random order. Energy expendi-
energy metabolism and satiety. Hormones including
ture measurements were conducted before and for 6 h after
cholescytokinin, peptide YY, gastric inhibitory peptide,
consumption of the meal. Total EE was 48 and 65% greater in
neurotensin and pancreatic polypeptide have been pro- posed to be involved in the mechanism by which MCT may
lean and obese individuals, respectively, after MCT compared
induce satiety; however, the exact mechanisms have not
with LCT consumption. Similar results were obtained by
been established. From the literature reviewed, we con-
Seaton et al. (4) comparing the effects of MCT or CO on EE
clude that MCT increase energy expenditure, may result in
after a single meal. Energy expenditure peaked at 16% above
faster satiety and facilitate weight control when included in
baseline after MCT consumption compared with 5% for CO. the diet as a replacement for fats containing LCT.
Dulloo et al. (5) investigated the thermogenic effects of
132: 329 –332, 2002.
low-to-moderate amounts of MCT consumption in healthy
adult men. Subjects were required to spend 24 h in a respira-
KEY WORDS: ● medium-chain triglycerides ●
tory chamber on four separate occasions; during that time,
diets differed in the ratio of MCT:LCT (0:30, 5:25, 15:15,30:0) provided as added fat. The diet was given at a level 1.4times energy requirements and the 30 g of added fat was
Fats varying in fatty acid chain lengths are metabolized differ-
distributed evenly across all meals. The authors found that EE
ently (1– 8). Medium-chain triglycerides (MCT),3 containing
between 0800 and 2300 h increased by 45, 135 and 265 kJ
6 –12 carbon fatty acids, differ from long-chain triglycerides
with 5, 15 and 30 g of MCT in the diet, respectively. Mean
(LCT), which have fatty acids of Ͼ 12 carbons, in that they are
24-h EE also increased by 162 and 475 kJ with 15 and 30 g of
absorbed directly into the portal circulation and transported to
MCT in added fat, respectively. Thus, the greater effects ofMCT than LCT on EE are evident not only in the few hoursafter the meal but for a much longer time.
1 Manuscript received 16 October. Revision accepted 18 December 2001.
Most results (3–5) from single-day experiments indicated that
2 To whom correspondence should be addressed.
replacing LCT for MCT in the diet could produce weight loss
after prolonged consumption. However, when Flatt et al. (6)
Abbreviations used: BW, body weight; CCK, cholecystokinin; CO, corn oil;
DVZ, Devazepide; EE, energy expenditure; FO, fish oil; GIP, gastric inhibitory
compared diets rich in MCT, LCT and low in fat, they concluded
peptide; LCFA, long-chain fatty acids; LCT, long-chain triglycerides; MCFA, me-
that a low fat diet was more prudent when aiming for weight loss.
dium-chain fatty acids; MCT, medium-chain triglycerides; PYY, peptide YY;
However, MCT consumption resulted in greater EE at several
SCFA, short-chain fatty acids; SCT, short-chain triglycerides; TEF, thermic effectof food; TG, triglycerides.
time points compared with the low fat diet.
0022-3166/02 $3.00 2002 American Society for Nutritional Sciences.
Few trials have been conducted over longer periods. One of
contrast, data from White et al. (8), who studied women,
those studies examined energy balance during the overfeeding of
found differences in EE of 138 kJ/d between MCT and LCT
liquid formula diets containing MCT (61% octanoate, 32% de-
consumption. Our own work with overweight women also
canoate) or LCT (32% oleate, 51% linoleate) for 7 d (7). EE was
revealed a difference in EE of ϳ188 kJ/d (18). From these
measured on d 1 and 6 for 10–15 min every 30 min for 6 h after
preliminary data, it appears that women respond less readily to
meal consumption. The thermic effect of food (TEF) was iden-
tified as 8% of ingested energy after MCT consumption comparedwith 5.8% after LCT consumption on d 1. After 6 d, TEF was 12
Effect of MCT on Food Intake and Satiety. Animal
and 6.6% of ingested energy with MCT and LCT consumption,
studies. Lower weight gain and decreased fat depot size with
respectively, indicating that the difference in EE between MCT
MCT feeding compared with LCT feeding in animals have
and LCT persists even after a week of overfeeding.
been attributed to two different effects of MCT, i.e., increased
The study of longest duration (14 d) published to date (8)
EE and decreased food intake. Satiety may also be affected by
sought to determine whether fatty acid chain length influ-
fatty acid chain length of dietary fat. Bray et al. (19) observed
enced EE and substrate oxidation in women. Subjects con-
greater feed intake when LCT were included in the diets of the
sumed a controlled, weight maintenance diet containing 40%
rats compared with diets containing MCT. After 80 d of
of energy as fat, either in the form of butter and coconut oil
consuming diets containing 60% of energy from CO, MCT or
(MCT; 38.9% of fatty acids contained chains with Ͻ16 car-
a mixture of the two, rats fed the CO and the CO-MCT diets
bons) or beef tallow. Energy expenditure was measured before
had a higher BW than those fed the MCT diet alone. Rats fed
and for 5.5 h after breakfast. Postprandial total EE after MCT
the MCT diet consumed less energy, and the authors con-
consumption was greater than after LCT consumption on d 7
cluded that -hydroxybutyrate may play a role in the differ-
but not d 14. The authors concluded that the effects of MCT
ence in food intake between MCT- and CO-fed rats.
Given these results, Maggio and Koopmans (20), in 1982,
All animal studies (9 –11) and most human studies (3–
conducted a study to clarify the origin and the nature of the
5,7,8) have shown that MCT consumption increases EE com-
signals that terminate short-term food intake of mixed meals
pared with a meal containing LCT. Investigators who found
containing triglycerides (TG) with fatty acids of different
the greatest differences also concluded that MCT could be
chain lengths. Sprague-Dawley rats were intubated intragas-
used in the treatment or prevention of human obesity (3–5).
trically and given free access to a liquid diet containing 21%
However, the studies conducted to date have been short,
of energy as fat. The TG infusions consisted of 70% TG
ranging from a single meal (3– 6) to several days (7,8).
(tributyrin, tricaprylin or triolein in different concentrations)
Whether effects of MCT on EE and RQ are long lasting and
and 30% carbohydrate. Shifting chain length from medium to
result in actual measurable and sustainable changes in body
long did not differentially affect food intake when the infu-
composition of humans remain to be established.
sions were equicaloric. Therefore, the authors concluded that
satiety may be related to the amount of energy ingested rather
Effect of MCT on Fat Deposition. Given that feed effi-
than to the physical characteristics of the specific nutrients.
ciency studies in animals and energetic studies in humans
This was in contrast to results obtained by Denbow et al. (21)
indicate enhanced EE after MCT consumption (3–11), addi-
who infused intrahepatically or intubated intragastrically
tional work has examined whether increased EE translates into
white leghorn cockerels with isoenergetic quantities of tribu-
decreased fat mass. In animals consuming MCT, BW were
tyrate, tridecanoate or trioleate and measured feed consump-
lower, fat depots smaller (12–15) and adipocyte size smaller
tion. Feed consumption with SCT and MCT infusion was
(12,13) with MCT compared with LCT consumption. These
suppressed within 1 h after intrahepatic infusion until 180
results led the authors to conclude that MCT could potentially
min. However, when infusions were given intragastrically,
prevent (13) or control (15) obesity in humans. However,
only SCT decreased feed intake. The authors concluded that
MCT consumption was not observed by Hill et al. (16) to
these results reflect the relatively rapid rate of digestion and
cause greater weight loss than lard, CO or fish oil (FO). Body
absorption of short-chain fatty acids (SCFA) from the gut
adipose tissue during the first 3 mo was not different among
along with oxidation of SCFA by the liver.
groups but after 6 mo, the group fed FO had less body fat than
Furuse et al. (22) also investigated the effects of two dif-
all other groups. Although both FO and MCT feeding resulted
ferent levels of MCT on feed intake in rats. They further
in small fat cells, only FO feeding was associated with inhibi-
examined the capacity of endogenous cholecystokinin (CCK)
to modulate feed intake with MCT. Feed intake of male
Only one study evaluated the ability of MCT to facilitate
Wistar rats fed diets containing CO, MCT or a 1:1 mixture of
weight reduction in humans (17). Obese women (n ϭ 16)
CO and MCT was determined every hour for 12 h and then at
consumed MCT (58% octanoate, 22% decanoate) or LCT
2-h intervals for the following 12 h. In a separate trial, Devaz-
(soy oil) in random order for either 4 wk if they were inpa-
epide (DVZ), a CCK-A receptor antagonist, was injected
tients or 12 wk if they were outpatients, at a level of 191 kJ/d.
intraperitoneally 40 min before feeding and feed intake was
There were no differences in weight loss or rate of weight loss
measured at 1, 2, 3 and 6 h postinjection. Feed intake de-
between diet treatments. A liquid diet containing 24% of
creased in a dose-dependent manner with increased concen-
energy as MCT failed to increase the rate of weight loss
tration of MCT in the diet and was enhanced 2 h after DVZ
compared with LCT. This lack of agreement with animal trials
injection. After 3 h, intake of the MCT diet was less than that
and EE experiments may have been due to the low fat content
of the CO diet. The authors thus concluded that satiety is
of the diets (1.5 g of total fat/d, of which 1.2 g was treatment
affected by carbon chain length in dietary TG sources.
fat) or to gender differences in the effects of MCT. Differencesdetected in EE with MCT and LCT consumption are consid-
Effect of MCT on Food Intake and Satiety. Human
erably greater in males than females. When data are extrapo-
studies. If MCT consumption enhances satiety and decreases
lated from trials conducted in men (3–5,7), average EE was
food intake in animals, an equivalent response might be ex-
ϳ460 kJ/d greater with MCT than with LCT consumption,
pected in humans. Stubbs and Harbron (23) examined
with a peak difference between treatments of 669 kJ/d (7). In
whether the effects of ingesting MCT can limit the hyperpha-
MEDIUM-CHAIN TRIGLYCERIDES AND WEIGHT MAINTENANCE
gia associated with high fat, energy-dense diets in humans. Six
inhibits gastric acid secretion in humans, is involved in the
men participated in a three-phase inpatient trial in which they
enterogastrone effect of MCFA. These investigators had pre-
had free access to experimental high fat foods (61.5% of
viously observed that infusions of MCFA suppressed gastrin-
energy as fat) for 14 d. Each experimental phase differed in the
stimulated gastric acid secretion without the involvement of
amount of MCT included in the diet, i.e., low, medium or high
CCK (28). Men (n ϭ 14) were intraduodenally infused for
MCT content with 20, 31 and 40%, respectively, of total
2.5 h with MCFA (56% octanoate, 43% decanoate), LCFA
energy as MCT. Subjects consumed 15.1 and 17.6 MJ less with
(CO) or saline in random order. The energy loads differed
the diet containing the most MCT compared with the diets
between MCFA and LCFA infusions, with the former provid-
containing the low and medium amounts of MCT, respec-
ing a load of 11.6 kJ/min and the latter providing a load of 22.7
tively, over the 14-d period. Body weights during consumption
kJ/min. Both infusions increased plasma levels of PYY; how-
of the low and medium MCT diets increased by 0.45 and 0.41
ever, LCFA resulted in a greater increase than MCFA infusion
kg, respectively, and decreased by 0.03 kg with the high MCT
(10.3 vs. 2.8 pmol/L). LCFA inhibited gastrin-stimulated gas-
content diet. Food and energy intakes were thus suppressed
tric acid secretion by 4.1 mmol/15 min compared with 2.7
when two thirds of the fat content of a high fat diet was
mmol/15 min for MCFA. PYY is therefore involved in the
derived from MCT, but BW were not affected.
enterogastrone effect of MCFA; however, MCFA are less
Another clinical trial (24) was designed to establish the
potent at inducing PYY release than LCFA. Greater induction
influence of chain length and degree of saturation on food
of PYY release by LCFA may be due to CCK discharge by
intake in normal-weight men. Breakfasts differing in the na-
LCFA because CCK has been shown to stimulate PYY secre-
ture of the fat, i.e., olive oil, lard, MCT or a fat substitute, were
tion. Other hormones may therefore be involved in the mech-
served and food intakes at lunch and dinner were measured.
anism by which MCFA inhibit gastric acid secretion. How-
Energy intake at lunch was lower after the MCT-containing
ever, except for GIP, which is not released in response to
breakfast than after all other breakfasts (3100 vs. 3715 kJ with
the fat substitute, 3278 kJ with olive oil and 3798 kJ with lard)
Recently, Feinle et al. (29) investigated the ability of TG
but there were no differences in food consumption at dinner.
with fatty acids of varying chain lengths to induce gastroin-
testinal sensations and symptoms. Five different infusions were
Hormones Iinvolved in the Satiating Effect of MCT
studied as follows: LCT (soybean oil), MCT, soy lecithin,
and LCT. Clinical trials (23,24) have shown that MCT
Orlistat and sucrose polyester. LCT and MCT both increased
consumption can lead to lower energy intakes but have not
gastric volume, with LCT causing the greater increase. All
explored the underlying mechanism. More recently, research
infusions resulted in increased feelings of fullness, bloating and
has focused on specific hormones that may be involved in the
nausea, and decreased hunger but effects were most pro-
satiating effect of MCT. McLaughlin et al. (25) examined the
nounced with the LCT infusion. The authors concluded that
relationship among fatty acid chain length, CCK secretion,
the mechanism of action of fat in the generation of gastroin-
and proximal and distal gastric motor function. Healthy vol-
testinal symptoms required digestion of TG. Furthermore, be-
n ϭ 15) were studied for their response to a control
cause MCT do not release CCK, but do affect sensations of
meal and orogastric infusion of 250 mL of a 0.05 mol/L fatty
fullness, bloating and nausea, CCK-dependent and CCK-in-
acid emulsion. Fatty acid emulsions containing fatty acids of
dependent mechanisms must be involved.
11 carbon chains and less did not increase plasma CCK con-
In humans, MCFA do not stimulate CCK secretion. There-
centrations compared with the vehicle, whereas long-chain
fore, CCK must not be the hormone responsible for their
fatty acids (LCFA) did. This study showed that the human
satiating effect (25–29). Although MCT have been shown to
proximal gut differentiates between fatty acid molecules; how-
induce satiety and to stimulate hormone secretion, no single
ever, it does not support the role of CCK in mediating the
hormone has been found to be strongly secreted due to MCT
digestion. PYY has been found to be secreted in response to
Several other studies have also reported that MCT do not
MCFA, yet it is still more potently secreted in response to
stimulate CCK secretion in humans (26 –28), and trials have
attempted to establish which hormone is responsible for theobserved effects of MCT on food intake. Barbera et al. (26)
Potential Benefits to Consumption of MCT on Body
compared effects of MCT and LCT on sensations of satiety,
Weight. There is evidence to suggest that short-term con-
gastric tone, gastric inhibitory peptide (GIP), pancreatic
sumption of MCT increases EE in humans (3–5,7,8) and
polypeptide and CCK. Subjects (n ϭ 9) were infused with
results in decreased fat cell size and body weight accretion in
saline, LCFA (mainly oleate and linoleate) or MCFA (octano-
animals (12–16,19). Human studies have shown that replacing
ate and decanoate) on three separate occasions in random
dietary LCT with MCT increases daily energy expenditure
order. LCFA infusion resulted in a greater rise in satiation
from 100 (6) to 669 kJ (7) in men and 138 kJ/d (8) in women.
than MCFA, but there was no difference between the two fats
Studies examining the satiating effect of fats of different chain
on the perception of fullness and bloating. The rise in gastric
lengths found that energy intake was ϳ1070 kJ lower when
volume was also greater with LCFA infusion than MCFA
meals contained MCT than when they contained LCT as the
infusion. Similarly, LCFA increased baseline levels of plasma
fat source (23). Van Wymelbeke et al. (24) found that intakes
CCK, GIP, neurotensin and pancreatic polypeptide compared
were 175– 698 kJ lower, depending on the chain saturation of
with saline, whereas MCFA infusion did not. The authors thus
the LCT, at the subsequent meal when MCT were substituted
concluded that MCFA induce gastric relaxation without in-
for LCT. Therefore, in the most optimistic scenario in which
creasing satiation or plasma levels of gut hormones. However,
EE would be increased by 669 kJ/d (7) and intakes decreased
because Stubbs and Harbron (23) and Van Wymelbeke (24)
by 698 kJ/d (23), a weight gain of 1.35 kg/mo could be avoided
have shown lower food intakes with diets rich in MCT, it is
by replacing LCT with MCT in the diet. On the other hand,
likely that other factors play a role in regulating energy bal-
the least optimistic scenario would give an increase in daily EE
of 100 kJ (6) and decreased daily food intake of 350 kJ/d (2
Maas et al. (27) examined effects of MCFA and LCFA on
subsequent meals, each less by 175 kJ) (24). In this case, a
peptide YY (PYY) release to determine whether PYY, which
weight gain of 0.45 kg/mo would be avoided (Fig. 1). If we
to-moderate amounts of medium-chain triglycerides: a dose-response study inhuman respiratory chamber. Eur. J. Clin. Nutr. 50: 152–158.
6. Flatt, J. P., Ravussin, E., Acheson, K. J. & Jequier, E.
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7. Hill, J. O., Peters, J. C., Yang, D., Sharp, T., Kaler, M., Abumrad, N. N. &
Thermogenesis in humans during overfeeding with me-
dium-chain triglycerides. Metabolism 38: 641– 648.
8. White, M. D., Papamandjaris, A. A. & Jones, P.J.H.
postprandial energy expenditure with medium-chain fatty acid feeding is attenu-ated after 14 d in premenopausal women. Am. J. Clin. Nutr. 69: 883– 889.
9. Lasekan, J. B., Rivera, J., Hirvonen, M. D., Keesey, R. E. & Ney, D. M.
Energy expenditure in rats maintained with intravenous or intragastric
infusion of total parenteral nutrition solutions containing medium- or long-chaintriglyceride emulsions. J. Nutr. 122: 1483–1492.
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15. Lavau, M. M. & Hashim, S. A.
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16. Hill, J. O., Peters, J. C., Lin, D., Yakubu, F., Greene, H. & Swift, L.
(EE) and satiety in humans. Energy expenditure can be increased by up
Lipid accumulation and body fat distribution is influenced by type of dietary fat fed
to 460 kJ/d and food intake decreased by 175– 698 kJ/d. The combi-
to rats. Int. J. Obes. 17: 223–236.
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18. St-Onge, M.-P., Bourque, C., Papamandjaris, A. A., Jones, P.J.H.
Consumption of medium chain triglycerides versus long chain triglycer-
project these data to long-term weight balance, a negative
ides over 4 weeks increases energy expenditure and fat oxidation in obese
weight balance of 5.4 –16.2 kg/y would be produced. However,
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19. Bray, G. A., Lee, M. & Bray, T. L.
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20. Maggio, C. A. & Koopmans, H. S.
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22. Furuse, M., Choi, Y. H., Mabayo, R. T. & Okumura, J. I.
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23. Stubbs, R. J. & Harbron, C. G.
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