The effects of 2-week ingestion of (−)-hydroxycitrate and (−)-hydroxycitrate combined with medium-chain triglycerides on satiety, fat oxidation, energy expenditure and body weight

Department of Human Biology, Maastricht University, Maastricht, The Netherlands.
International Journal of Obesity (Impact Factor: 5). 08/2001; 25(7):1087-94. DOI: 10.1038/sj.ijo.0801605
Source: PubMed
Assessment of the effect of 2-week supplementation with (--)-hydroxycitrate (HCA) and HCA combined with medium-chain triglycerides (MCT) on satiety, fat oxidation, energy expenditure (EE) and body weight (BW) loss.
Three intervention periods of 2 weeks separated by washout periods of 4 weeks. Double-blind, placebo-controlled, randomised and cross-over design.
Eleven overweight male subjects (mean+/-s.d.; age, 47+/-16 y; body mass index, 27.4 +/- 8.2 kg/m(2)).
Subjects consumed three self-selected meals and four iso-energetic (420 kJ) snacks daily with either no supplementation (PLA), 500 mg HCA (HCA) or 500 mg HCA and 3 g MCT (HCA+MCT). Each intervention ended with a 36 h stay in the respiration chamber.
There was a significant BW loss during the 2 weeks of intervention (PLA, -1.0 +/- 0.4 kg, P<0.05; HCA, -1.5 +/- 0.5 kg, P<0.01; HCA+MCT, -1.3 +/- 0.2 kg, P<0.001), but this reduction was not different between treatments. 24 h EE (PLA, 11.8 +/- 0.2 MJ; HCA, 11.7 +/- 0.1 MJ; HCA+MCT, 11.5 +/- 0.1 MJ), 24 h RQ (0.85 +/- 0.00 in all treatments) and the area under the curve of the appetite-related parameters were not different between treatments.
Two-week supplementation with HCA and HCA combined with MCT did not result in increased satiety, fat oxidation, 24 h EE or BW loss compared to PLA, in subjects losing BW.


Available from: Eva M R Kovacs, Nov 27, 2014
The effects of 2-week ingestion of (ÿ
and (ÿ
)-hydroxycitrate combined with medium-chain
triglycerides on satiety, fat oxidation, energy
expenditure and body weight
EMR Kovacs
*, MS Westerterp-Plantenga
and WHM Saris
Department of Human Biology, Maastricht University, Maastricht, The Netherlands
OBJECTIVE: Assessment of the effect of 2-week supplementation with (ÿ)-hydroxycitrate (HCA) and HCA combined with
medium-chain triglycerides (MCT) on satiety, fat oxidation, energy expenditure (EE) and body weight (BW) loss.
DESIGN: Three intervention periods of 2 weeks separated by washout periods of 4 weeks. Double-blind, placebo-controlled,
randomised and cross-over design.
SUBJECTS: Eleven overweight male subjects (mean s.d.; age, 47 16 y; body mass index, 27.4 8.2 kg=m
INTERVENTION: Subjects consumed three self-selected meals and four iso-energetic (420 kJ) snacks daily with either no
supplementation (PLA), 500 mg HCA (HCA) or 500 mg HCA and 3 g MCT (HCA MCT). Each intervention ended with a 36 h
stay in the respiration chamber.
RESULTS: There was a signi®cant BW loss during the 2 weeks of intervention (PLA, ÿ1.0 0.4 kg,
< 0.05; HCA, ÿ1.5 0.5 kg,
< 0.01; HCA MCT, ÿ1.3 0.2 kg,
< 0.001), but this reduction was not different between treatments. 24 h EE (PLA,
11.8 0.2 MJ; HCA, 11.7 0.1 MJ; HCA MCT, 11.5 0.1 MJ), 24 h RQ (0.85 0.00 in all treatments) and the area under
the curve of the appetite-related parameters were not different between treatments.
CONCLUSION: Two-week supplementation with HCA and HCA combined with MCT did not result in increased satiety, fat
oxidation, 24 h EE or BW loss compared to PLA, in subjects losing BW.
International Journal of Obesity
(2001) 25, 1087±1094
Keywords: (ÿ)-hydroxycitrate; medium-chain triglycerides; satiety; energy expenditure; body weight loss
The increasing incidence of obesity is a recognised medical
problem in developed countries.
Obesity is the net result
of disrupted balance between energy intake and energy
the excess being stored in the adipose tissue. It is
a major factor for a number of diseases, including coronary
heart diseases, hypertension, type 2 diabetes mellitus, pul-
monary dysfunction, osteoarthritis and certain types of
Treatment of obesity is often unsuccessful.
Weight loss can be achieved, but long-term weight main-
tenance after weight loss is rarely shown.
Therefore, iden-
ti®cation of substances that improve or at least sustain
satiety during energy restriction is needed. One possible
way to improve satiety is to increase hepatic fatty acid
oxidation. Evidence for a role of hepatic fatty acid oxidation
in the control of eating has been shown in animals.
fore, ®nding ways to stimulate fatty acid oxidation in the
liver should be promising for appetite and weight control.
We hypothesise that stimulation of the post-ingestive fatty
acid oxidation could modulate fat-induced satiety. We there-
fore investigated the potential of (ÿ)-hydroxycitrate (HCA)
and medium-chain triglycerides (MCT), which are believed
to induce fatty acid oxidation,
to increase satiety and
decrease body weight.
HCA is an active ingredient that is extracted from the rind
of the fruit Garcinia cambogia, a native species to India, and is
promoted as a weight loss agent. HCA is an inhibitor of
ATP-citrate-lyase, a cytosolic (extramitochondrial) enzyme
that catalyses the cleavage of citrate to oxaloacetate and
HCA might induce satiety by inhibiting
*Correspondence: EMR Kovacs, Department of Human Biology,
Maastricht University, PO Box 616, 6200 MD Maastricht,
The Netherlands.
E-mail: E.Kovacs@HB.UNIMAAS.NL
Received 26 July 2000; revised 27 November 2000;
accepted 3 January 2001
International Journal of Obesity (2001) 25, 1087±1094
ß 2001 Nature Publishing Group All rights reserved 0307±0565/01 $15.00
International Journal of Obesity (2001) 25, 1087±1094
ß 2001 Nature Publishing Group All rights reserved 0307±0565/01 $15.00
Page 1
malonylCoA formation, which in turn would stimulate car-
nitine transferase activity, resulting in decreased fat synthesis
and increased fat oxidation
or by increasing the rate of
hepatic glycogen synthesis.
Furthermore HCA might pro-
mote weight maintenance by inhibiting or limiting de capa-
city for de novo lipogenesis,
especially along with a high
carbohydrate diet. Up to now, however, the results on the
effects of HCA on appetite, body weight and energy expen-
diture and its possible contribution as a weight loss agent in
humans are controversial.
Several studies found a posi-
tive effect of HCA administration alone or in combination
with other ingredients on appetite, energy intake, body
weight loss, fat oxidation or energy expenditure,
others did not.
To distinguish the satiety effect of HCA
from the fatty acid oxidation effect, we conducted two
separate studies. In our previous study we found no effect
of HCA on satiety in subjects losing body weight.
In the
present study, we concentrate on the possible effects of
chronic HCA administration on fatty acid oxidation.
Medium-chain triglycerides (MCT) have been repeatedly
suggested as a food ingredient that may contribute to the
control of body weight. MCT are known to be rapidly
hydrolysed and absorbed comparably to glucose.
Unlike long-chain triglycerides (LCT) that are transported
in chylomicrons through the lymphatic system, MCT are
converted into medium-chain fatty acids (MCFA) that
directly enter the blood through the portal system. MCFA
can cross the inner mitochondrial membrane in the liver and
muscle independently of the acylcarnitine transferase
Studies showed that fatty acids delivered by MCT
are preferentially oxidised and poorly stored within tissues,
and that MCT have a marked thermic effect.
In addition to
that, MCT have been shown to have satiating properties and
to decrease food intake compared to LCT
by involving
a cascade of pre-absorptive and post-absorptive mechanisms.
However, the exact mechanism underlying the reduction in
food intake after MCT ingestion is not fully understood.
The aim of the present study was to investigate the effects
of 2-week administration of HCA and HCA combined with
MCT on satiety, fat oxidation, energy expenditure and body
weight. We hypothesised that HCA supplementation might
affect appetite and body weight regulation by increasing fat
oxidation and metabolic rate, re¯ected by an increase in
energy expenditure. We further hypothesised that the com-
bination of HCA and MCT may have a stronger effect on
fatty acid oxidation and consequently on satiety compared
to HCA alone. In addition MCT could have a thermogenic
Eleven normal to moderately obese male subjects partici-
pated in this study. The subjects were recruited by advertise-
ments in local newspapers. Selection took place following
health criteria (no diabetes, no cardiovascular diseases, and
no medical treatment) and body weight (BW) criteria (body
mass index 25±31 kg=m
). Baseline characteristics of the
subjects are presented in Table 1. The subjects were not
HCA or MCT users. The nature and risks of the experimental
procedure were explained to the subjects, and all subjects
gave their written informed consent. The study was
approved by the Ethical Committee of Maastricht University.
Experimental design
The experiment had a double-blind, placebo-controlled,
randomised, cross-over design. The experimental design
consisted of three intervention periods of 2 weeks separated
by washout periods of 4 weeks. Each intervention period
ended with a 36 h stay in the respiration chamber.
During the washout periods, the subjects consumed a self-
selected and self-prepared diet. During the intervention
periods, the subjects consumed at home three self-selected
and self-prepared meals daily (breakfast, lunch, and dinner)
with no restriction regarding type and amount of food. They
were instructed to drink maximally one glass of alcoholic
beverage per day. Between the meals, the subjects consumed
an iso-energetic snack (cereal bar) of 22 g (energy, 420 kJ;
protein, 0.7 g; fat, 4 g; carbohydrate, 14 g; dietary ®bre, 0.5 g)
with no supplementation (PLA), with supplementation of
500 mg (ÿ)-hydroxycitrate (HCA; 850 mg SuperCitrimax
HCA 600 SXG, HCA content 58, 81%, EuroChem Feinchemie
GmbH, Mu
nchen, Germany) or 500 mg (ÿ)-hydroxycitrate
and 3 g medium-chain triglycerides (HCA MCT). The
dosage used was similar or higher to that used in other
studies in which an effect of HCA on BW reduction was
found (3 500 mg=day;
2 55±110 mg=day
). The
snacks were consumed at four ®xed time points: 1 h before
lunch, 2 h after lunch, 1 h before dinner and 2 h after dinner.
Between the meals, the subjects were not allowed to eat with
exception of the prescribed snacks. They were allowed to
drink ad libitum water, coffee and tea (without sugar and
milk). During the last 3 days of each intervention, the
subjects were instructed to consume no alcohol and to eat
Table 1 Subject characteristics at baseline
Mean s.d. Range
Age (y) 47 16 27±56
Height (m) 1.77 0.51 1.71±1.85
Weight (kg) 85.4 25.8 73.4±98.6
Body mass index (kg=m
) 27.4 8.2 24.5±31.4
Waist circumference (cm) 94 28 86±109
Hip circumference (cm) 102 30 90±111
Waist±hip ratio 0.93 0.27 0.83±1.04
Blood glucose (mmol=l) 5.21 1.59 4.81±5.62
Blood triglycerides (mmol=l) 1.32 0.70 0.44±2.05
F1 (cognitive restraint) 7 4 2±15
F2 (disinhibition) 4 31±8
F3 (hunger) 3 20±6
Herman±Polivy restraint 16 6 10±21
11 men. F1±F3,
factors 1±3
of the Three Factor Eating Questionnaire.
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 2
ad libitum food that was supplied from our laboratory for
breakfast, lunch and dinner. The food had a food quotient
(FQ) of 0.85.
Body weight was measured during screening, at the begin-
ning, after 1 week and at the end of each intervention period
on a digital balance accurate to 0.02 kg (Chyo-MW-150K,
Japan) with subjects in underwear, in the fasted state and
after voiding their bladder. Height was measured to the
nearest 0.1 cm during screening using a wall-mounted
stadiometer (Seca, model 220, Hamburg, Germany). The
body mass index was calculated by BW=height
The distribution of fat was investigated during screening
by measuring the waist and hip circumferences and calcula-
tion of the waist±hip ratio (WHR). The waist circumference
was measured at the site of the smallest circumference
between the rib cage and the ileac crest, with the subjects
in standing position. The hip circumference was measured at
the site of the largest circumference between the waist and
the thighs. The WHR was calculated by dividing the waist
circumference by the hip circumference.
Body composition was measured at the beginning and at
the end of each intervention period by hydrodensitometry
and deuterium (
O) dilution technique
and was calcu-
lated using the combined equation of Siri.
Body weight was
measured in the fasted state with a digital balance accurate to
0.01 kg (Sauter Typ E1200, Ebingen, Germany). Whole body
density was determined by underwater weighing with simul-
taneous assessment of long volume residual with the helium
dilution technique using a spirometer (Volugraph 2000,
Mijnhardt, The Netherlands). Measurements were performed
in triplicate and the average was used to calculate body
density. The dilution of the deuterium isotope is a measure
for total body water (TBW).
Subjects were asked to collect a
urine sample in the evening just before drinking a weighed
amount of deuterium enriched water solution. After inges-
tion of the deuterium solution no further ¯uid or food
consumption was permitted. Ten hours after ingestion of
the deuterium solution a second urine sample (second void-
ing) was collected. Deuterium concentration in the urine
samples was measured using an isotope ratio mass spectro-
meter (Micromass Optima, Manchester, UK). TBW was
obtained by dividing the measured deuterium dilution
space by 1.04.
Fat-free mass (FFM) was calculated by divid-
ing the TBW by the hydration factor 0.73. By subtracting
FFM from BW, fat mass was obtained. Fat mass expressed as a
percentage of BW revealed body fat percentage.
Eating behaviour
Eating behaviour was analysed during screening, during the
®rst and the last day of each intervention period using a
validated Dutch translation of the Three Factor Eating Ques-
tionnaire (TFEQ).
Cognitive restrained and unrestrained
eating behaviour (factor 1), emotional eating and disinhibi-
tion (factor 2) and the subjective feeling of hunger (factor 3)
were scored. Body weight concern and chronic dieting
behaviour were investigated with the Herman Polivy
questionnaire (HP).
Blood parameters
At the beginning and at the end of each intervention period,
a fasting blood sample of 10 ml was obtained and mixed with
EDTA to prevent clotting. Plasma was obtained by centrifu-
gation (4
C, 3000 rpm, 10 min) and stored at ÿ 80
C until
analysis of glucose by a hexokinase method (Roche Diagnos-
tics, Hoffmann-La Roche, Basel, Switzerland), triglycerides
(GPO-trinder 337, Sigma), free fatty acids by an ACS-ACOD
method (Wako chemicals, Neuss, Germany), glycerol by a
glycerolkinase-lipase method (Boehringer, Mannheim,
Germany), b-hydroxybutyrate (BHB) by the method of
Moore et al
using a semi-automated centrifugal spectro-
photometer (Cobas Fara, Roche Diagnostics), and insulin
with ELISA (Mercodia 10-1113-01).
Daily energy intake
Energy intake over the previous week was recorded at the
beginning and at the end of each intervention period using
a food frequency questionnaire. Personal instruction was
given in advance. The food frequency questionnaires were
analysed using the Dutch food composition table
and the
accessory computer program (Becel Nutrition Program
Daily energy intake before intervention and during the
second week of intervention was compared with predicted
24 h energy expenditure
that amounted on average
12.0 1.1 MJ=day. Since predicted 24 h energy expenditure
was signi®cantly higher compared to the reported energy
intakes (before intervention: PLA, 6.9 0.4 MJ=day; HCA,
6.5 0.4 MJ=day; HCA MCT, 7.1 0.5 MJ=day; during the
second week of intervention: PLA, 7.5 0.5 MJ=day;
HCA, 7.9 0.3 MJ= day; HCA MCT, 8.6 0.5 MJ=day) and
mean changes in reported energy intake were not related to
mean changes in body weight (r 0.04; P > 0.05), these data
were not used for further analysis.
Changes in mood during intervention were scored on
anchored 100 mm visual analogue scales at the beginning
and at the end of each intervention period.
Tolerance of the snacks was determined at the end of each
intervention period using a questionnaire on occurrence of
gastrointestinal and other complaints and scored on a 5
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 3
points scale (0 not at all, 1 less, 2 sometimes,
3 relatively much, 4 very much).
Indirect calorimetry
Oxygen consumption and carbon dioxide production were
measured in a whole room calorimeter.
The respiration
chamber was a 14 m
room, furnished with a bed, chair,
computer, television, radio-cassette player, telephone, inter-
com, sink and toilet. The room was ventilated with fresh air
at a rate of 70±80 l=min. The ventilation rate was measured
with a dry gas meter (Schlumberger, type 4, the Netherlands).
The concentration of oxygen and carbon dioxide was mea-
sured using a paramagnetic O
analyser (Hartmann & Braun,
type Magnos 6G, Germany; Servomex, type OA184A, UK)
and an infrared CO
analyser (Hartmann and Braun, type
Uras 3G, Germany). During each 15 min period, six samples
of outgoing air for each chamber, one sample each of fresh
air, zero gas and calibration gas were measured. The gas
samples to be measured were selected by a computer that
also stored and processed the data.
Physical activity
In the respiration chamber subjects followed a protocol
consisting of ®xed times for breakfast, lunch and dinner,
sedentary activities and bench stepping exercise. The bench
stepping exercise was performed three times a day (10:30 h,
14:30 h, and 20:30 h) for 30 min at intervals of 5 min exercise
alternated with 5 min rest, at a rate of one step per second
with a bench height of 25 cm. Apart from the exercise
protocols, subjects were not restricted in their activities,
only sleeping and strenuous physical activity were not
allowed. Physical activity was monitored using a radar
system working on the Doppler principle.
Energy intake
Before entering the respiration chamber, the subjects con-
sumed ad libitum a standardised dinner (pasta meal; energy,
393 kJ=100 g; protein, 3.8 g=100 g; carbohydrate, 11.1 g=100 g;
fat, 3.8 g=100 g) and food intake was determined.
Energy intake (EI), adapted to reach energy balance, was
determined from 24 h sleeping metabolic rate (SMR) mea-
sured during the ®rst night and multiplied by an activity
index of 1.6.
The subjects received a diet divided over three
meals (breakfast at 08:30 h, lunch at 12:00 h and dinner at
18:00 h) and four snacks (1 h before and 2 h after lunch, 1 h
before and 2 h after dinner). The food had a FQ of 0.85.
Energy expenditure and substrate oxidation
Twenty four hour energy expenditure (24 h EE) consisted of
sleeping metabolic rate (SMR), diet-induced thermogenesis
(DIT) and activity-induced energy expenditure (AEE).
Twenty four hour EE and 24 h respiratory quotient (RQ)
were calculated from 07:00 h to 07:00 h, from oxygen con-
sumption and carbon dioxide production according to the
method of Weir.
SMR was measured on both nights and
was de®ned as the lowest mean EE measured over three
consecutive hours between 00:00 h and 07:00 h. The average
SMR of the two nights was used in further calculations. DIT
was calculated by plotting EE against radar output, both
averaged over 30 min periods. The intercept of the regression
line at the lowest radar output represented the energy
expenditure in the inactive state (resting metabolic rate,
RMR), consisting of SMR and DIT.
DIT was determined by
subtracting SMR from RMR. AEE was determined by sub-
tracting RMR from 24 h EE. Carbohydrate, fat and protein
oxidation was calculated using oxygen consumption and
carbon dioxide production and urinary nitrogen excretion:
Protein oxidation g=day6:25 N
Fat oxidation g=day1:718 VO
ÿ 1:718 VCO
ÿ 0:315 P
Carbohydrate oxidation g=day4:17 VCO
ÿ 2:965 VO
ÿ 0:390 P
where N is total nitrogen excreted in urine (g=day); VO
oxygen consumption (l=day); VCO
is carbon dioxide pro-
duction (l=day); P is protein oxidation (g=day).
Twenty-four hour urine was collected from the second
voiding on the day of the experiment until the ®rst voiding
of the following day. Samples were collected in containers
with 10 ml H
to prevent nitrogen loss through evapora-
tion. Volume and nitrogen concentration were measured,
the latter using a nitrogen analyser (Elemental Analyzer,
CHN-O-Rapid, Heraeus).
During the stay in the respiration chamber, appetite ratings
(hunger, satiety, fullness, desire to eat, appetite, anticipated
food intake and thirst) were scored on anchored 100 mm
visual analogue scales.
Questionnaires were completed at
10 ®xed time points, respectively immediately before and
after breakfast, in the morning at 10:30 h, immediately
before and after lunch, in the afternoon at 15:00 h, immedi-
ately before and after dinner, in the evening at 20:30 h, and
before sleeping at 23:30 h. Appetite ratings during 24 h stay
in the respiration chamber were expressed as area under the
curve (24 h AUC), corrected for the subject's minimum score.
Statistical analysis
Data are presented as mean standard error (s.e.). Differ-
ences between the treatments were determined by analysis of
variance for repeated measures (ANOVA) and Sheffe-F post hoc
test (Statview SE Graphics
). The measurements at the
beginning and at the end of the experiment were compared
using paired t-tests. Pearson correlation coef®cients, r, were
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 4
calculated to determine the relationship between selected
variables. The level of signi®cance was set at P < 0.05.
There was a signi®cant BW reduction during 2 weeks of
intervention (PLA, ÿ1.0 0.4 kg, P < 0.05; HCA, ÿ1.5
0.5 kg, P < 0.01; HCA MCT, ÿ1.3 0.2 kg, P < 0.001). How-
ever, BW reduction was not different between treatments.
BW loss was greater during the ®rst compared to the third
intervention period (ÿ2.0 0.5 kg vs ÿ0.5 0.2 kg; P < 0.05)
with values for the second intervention intermediate
(ÿ1.3 0.3 kg). Body fat decreased with HCA MCT
(ÿ0.9 0.4%, P < 0.05), but not with PLA and HCA
(ÿ0.6 0.8% and ÿ0.3 0.3%, respectively). However, no
difference in body fat loss was found between treatments.
Scores on the HP and the TFEQ questionnaires were
similar for all treatments and did not change during
Fasting plasma glucose concentration before and after
intervention was similar for each treatment. Plasma glucose
concentration was reduced as a result of intervention with
PLA (ÿ0.17 0.07 mmol=l; P < 0.05), but not with HCA and
HCA MCT (ÿ0.09 0.09 and ÿ0.08 0.09 mmol=l,
respectively). However, reduction in plasma glucose was
not different between treatments. Fasting plasma FFA, gly-
cerol, triglycerides and insulin concentrations before and
after intervention as well as changes during intervention
were similar between treatments. Fasting plasma BHB before
intervention was higher with HCA MCT compared to PLA
(P < 0.05). There was no difference in plasma BHB after
intervention or in plasma BHB change during intervention
between treatments.
There was no change in mood (relaxed, gloomy, pleasant,
angry, afraid, sad) during intervention, and no differences
were found between treatments. The snacks were similarly
tolerated in all treatments and values for complaints
remained low. Compliance to the snacks was determined
by asking the subjects how many snacks were left. A mean of
96% of the snacks was consumed, indicating a high com-
pliance to the snacks. Food intake during ad libitum meal
before entering the respiration chamber was similar for all
treatments (PLA, 2153 102 kJ; HCA, 2076 161 kJ;
HCA MCT, 2234 140 kJ).
Mean 24 h EI and 24 h EE during the stay in the respiration
chamber are presented in Figure 1. EI was chosen to reach
energy balance. However, the subjects tended to be in negative
energy balance (PLA, ÿ0.6 0.3 MJ; HCA, ÿ0.5 0.2 MJ;
HCA MCT, ÿ0.5 0.3 MJ; all P < 0.1), but the level of nega-
tive energy balance was not different between treatments.
There was no difference in SMR, RMR, DIT and AEE between
treatments (Figure 1). DIT was 7.7 1.3%, 8.9 3.2% and
7.7 1.3% of EI with PLA, HCA and HCA MCT, respectively
(NS). Calculated physical activity index, de®ned as EE divided
by SMR, was not different between treatments (PLA,
1.65 0.03; HCA, 1.62 0.02; HCA MCT, 1.61 0.02).
SMR was related to FFM with HCA MCT (r 0.67, P < 0.05),
and tended to be related to FFM with PLA and HCA (r 0.57
and r 0.62, respectively; P < 0.1; Figure 2). 24 h EE was not
related to FFM in any of the treatments (PLA, r 0.34; HCA,
r 0.52; HCA MCT, r 0.45; P > 0.05). There was no differ-
ence in protein (PLA, 82 4g=day; HCA, 81 3g=day;
HCA MCT, 74 4g= day), fat (PLA, 80 4g=day; HCA,
81 6g=day; HCA MCT, 77 3g=day) and carbohydrate
oxidation (PLA, 201 7g=day; HCA, 192 9g=day;
Figure 1 Twenty four hour energy intake and 24 h energy expenditure.
Values are means. PLA placebo; HCA (ÿ)-hydroxycitrate, MCT
medium-chain triglycerides; SMR sleeping metabolic rate; DIT diet-
induced thermogenesis; AEE activity-induced energy expenditure;
EI energy intake. Statistical signi®cance was determined by an analysis
of variance for repeated measures (ANOVA).
Figure 2 Relation between sleeping metabolic rate and fat-free mass.
PLA placebo; HCA (ÿ)-hydroxycitrate; MCT medium-chain trigly-
cerides. Relationship between variables was determined by calculating
Pearson correlation coef®cients. PLA,
< 0.1; HCA,
< 0.1; HCA MCT,
< 0.05.
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 5
HCA MCT, 202 7g=day) between trials. Twenty-four hour
RQ and non-protein RQ were similar in all trials (PLA,
0.85 0.00 and 0.85 0.00; HCA, 0.85 0.00 and
0.84 0.01; HCA MCT, 0.85 0.00 and 0.85 0.00,
The 24 h AUC of hunger, satiety, fullness, desire to eat,
appetite, anticipated food intake and thirst were similar in all
treatments. Satiety was higher with HCA compared to
HCA MCT before dinner and fullness was higher with PLA
compared to HCA before sleeping (P < 0.05). The subjects felt
thirstier with PLA compared to HCA after dinner (P < 0.05).
There was no difference at any time point in hunger, desire to
eat, appetite, and anticipated food intake between treatments.
In the present study, the potential of HCA and HCA combined
with MCT on satiety, fat oxidation, energy expenditure and
body weight was investigated in overweight men. The results
did not support the hypothesis that HCA supplementation
may be effective on appetite and weight control by increasing
fat oxidation, and that MCT may have an additional effect.
Results on the effect of HCA supplementation in humans
are controversial. Several studies found a positive effect of
HCA alone or in combination with other ingredients, (eg
chromium, caffeine, chitosan) on appetite,
24 h energy
and body weight loss.
However, other studies
did not ®nd a signi®cant effect of HCA on body weight.
HCA has been suggested to contribute to body weight loss by
increasing fat oxidation and inducing satiety. Until now, few
studies have investigated the effects of HCA ingestion on fat
oxidation and energy expenditure in humans. Kriketos et al
found no effect of 3 days HCA supplementation (3.0 g=day)
on fat oxidation and energy expenditure during rest or
moderate exercise in sedentary humans. Similarly, van
Loon et al
found no acute effect of HCA on energy expen-
diture and fat oxidation during rest and exercise in trained
subjects, even following ingestion of large quantities of HCA
(18.3 g). From these results, it may be argued that treatment
with HCA was not suf®ciently long and that HCA might
have an effect on fat oxidation or other parameters such as
appetite only over a longer investigation period. In the
present study, supplementation with HCA and HCA com-
bined with MCT lasted 2 weeks. However, no effect of HCA
on fat oxidation or 24 h energy expenditure was found, and
MCT did not result in an additional effect.
HCA administration has been shown to inhibit the rate of
lipogenesis in rodents
and to increase the rate of
hepatic glycogen synthesis,
but this has not been con-
®rmed in humans. An excess energy intake as carbohydrate
is needed to promote de novo lipogenesis and to increase
glycogen synthesis. However, the subjects who participated
in the present study were in a state of negative energy
balance. This is con®rmed by a body weight loss > 1kg
during the two weeks of intervention. Body weight loss
resulted from a food intake regimen that prescribed to refrain
from food consumption in between meals, with exception of
the four snacks and non-caloric beverages, and to minimise
alcohol intake. This negative energy balance may explain
why HCA was not effective in reducing appetite and inhibit-
ing fat synthesis as the conversion of citrate into acetylCoA
by ATP-citrate-lyase only occurs when energy intake exceeds
the energy requirements of the body. In other words, when a
low-energy diet did not meet the energy requirements of the
body, carbohydrate will be used in the citric acid cycle to
produce ATP for energy rather than to form citrate, the
substrate for de novo fatty acid synthesis. The results suggest
that HCA is not effective in inhibiting fat synthesis or
stimulating hepatic glycogen formation in a condition of a
moderate negative energy balance. The ineffectiveness of
HCA in dieting humans in fact has also been observed in
other studies.
Moreover, in a condition of energy bal-
ance, Westerterp-Plantenga and Kovacs
found that admin-
istration of HCA for two weeks resulted in reduced 24 h
energy intake on a subsequent test day.
In conclusion, it has been shown that, in circumstances
when two mechanisms which may play a role in the effec-
tiveness of HCA (ie de novo lipogenesis, hepatic glycogen
synthesis) are very likely excluded, the other mechanism
(ie fatty acid oxidation), which also might induce satiety, was
not present. If HCA is an effective food supplement in
relation to body weight regulation, it would probably be
effective by inhibiting de novo lipogenesis or by stimulating
hepatic glycogen synthesis. HCA may not be effective in
inhibiting de novo lipogenesis and stimulating hepatic glyco-
gen formation in a condition of negative energy balance and
body weight loss. HCA might therefore be effective in pre-
vention of weight (re)gain, and thus in prevention of obesity,
rather than in supporting body weight loss. Further con®r-
mation needs to be obtained from experiments on possible
effects of HCA on de novo lipogenesis and glycogen synthesis
during weight (re)gain in humans.
Supplementation with MCT did not result in an addi-
tional effect on satiety, 24 h energy intake, fat oxidation or
body weight. Studies showed that MCT have satiating prop-
erties and decrease food intake compared to LCT.
Wymelbeke et al
found that a breakfast supplemented with
MCT (ca 43 g) decreased energy intake during a free-choice
lunch. Rolls et al
found that a small preload of MCT (ca
18 g, 36 g or 54 g) incorporated into a liquid meal was more
effective at suppressing energy intake of a subsequent meal
presented 30 min later, compared to LCT, already with the
lowest dosage. In the present study, a lower dosage of MCT
(12 g=day) was used. This might explain why no effect of
MCT was found on energy intake. Studies also showed that
MCT increases thermogenesis and fat oxidation.
The sti-
mulating effect of MCT on energy expenditure was shown
with low dosages of MCT (15 and 30 g=day) but disappeared
at a dosage below 15 g=day.
This may indicate that the
dosage of MCT used in the present study was to low in order
to ®nd an effect on energy expenditure. Finally, we are
not able to make statements about the ef®cacy of MCT
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 6
themselves, as they were not investigated alone. Since HCA
was not effective in this study, it is possible that the possible
effect of MCT was inhibited.
We gratefully acknowledge Miranda de Vries, Joan Senden, and
Paul Schoffelen for their assistance. This study was supported
by Novartis Consumer Health Ltd, Nyon, Switzerland.
1 Seidell JC. Obesity in Europe. Obes Res 1995; 3(Suppl 2): 249s±259s.
2 Flatt JP, Ravussin E, Acheson KJ, Je
quier E. Effects of dietary fat on
postprandial substrate oxidation and on carbohydrate and fat
balances. J Clin Invest 1985; 76: 1019±1024.
3 Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an
independent risk factor for cardiovascular disease: a 26-year
follow-up of participants in the Framingham Heart Study. Circu-
lation 1983; 67: 968±977.
4 Kromhout D. Body weight, diet, and serum cholesterol in 871
middle-aged men during 10 years of follow-up (the Zutphen
Study). Am J Clin Nutr 1983; 38: 591±598.
5 Noppa H. Body weight change in relation to incidence of
ischemic heart disease and change in risk factors for ischemic
heart disease. Am J Epidemiol 1980; 111: 693±704.
6 Fogelholm M, Kukkonen-Harjula K, Oja P. Eating control and
physical activity as determinants of short-term weight main-
tenance after a very-low-calorie diet among obese women. Int J
Obes Relat Metab Disord 1999; 23: 203±210.
7 Pasman WJ, Saris WHM, Westerterp-Plantenga MS. Predictors of
weight maintenance. Obes Res 1999; 7: 43±50.
8 Westerterp-Plantenga MS, Kempen KP, Saris WHM. Determinants
of weight maintenance in women after diet-inducecd weight
reduction. Int J Obes Relat Metab Disord 1998; 22: 1±6.
9 Langhans W. Metabolic control of food intake. Role of the liver.
In: Westerterp-Plantenga MS, Steffen AB, Tremblay A (eds). Reg-
ulation of food intake and energy expenditure. EDRA: Milano; 1999.
pp 185±199.
10 Furuse M, Choi YH, Mabayo RT, Okumura JI. Feeding behavior in
rats fed diets containing medium chain triglyceride. Physiol Behav
1992; 52: 815±817.
11 Jeukendrup AE, Saris WHM, Wagenmakers AJM. Fat metabolism
during exercise: a review. Part III: The effects of nutritional
interventions. Int J Sports Med 1998; 19: 371±379.
12 McCarty MF. Reduction of free fatty acids may ameliorate risk
factors associated with abdominal obesity. Med Hypotheses 1995;
44: 278±286.
13 Rolls BJ, Gnisak N, Summerfeld A, Laster LJ. Food intake in dieters
and nondieters after a liquid meal containing medium-chain
triglycerides. Am J Clin Nutr 1988; 48: 66±71.
14 Satabin P, Auclair E, Servan E, Achagiotis CL, Guezennec CY.
In¯uence of glucose, medium-chain and long-chain triglyceride
gastric loads and forced exercise on food intake and body weight
in rats. Physiol Behav 1991; 50: 147±150.
15 Stubbs RJ, Harbron CG. Covert manipulation of the ratio of
medium- to long-chain triglycerides in isoenergetically dense
diets: effect on food intake in ad libitum feeding men. Int J Obes
Relat Metab Disord 1996; 20: 435±444.
16 Sullivan AC, Triscari J. Metabolic regulators as a control for lipid
disorders. I. In¯uence of (ÿ)-hydroxycitrate on experimentally
induced obesity in the rodent. Am J Clin Nutr 1977; 30: 767±776.
17 Watson JA, Fang M, Lowenstein JM. Tricaballylate and hydro-
xycitrate: substrate and inhibitor of ATP: citrate oxaloacetate
lyase. Arch Biochem Biophys 1969; 135: 209±217.
18 Sullivan AC, Hamilton JG, Miller ON, Wheatley VR. Inhibition of
lipogenesis in rat liver by (ÿ)-hydroxycitrate. Arch Biochem Bio-
phys 1972; 150: 183±190.
19 Szutowicz A, Stepien M, Lysiak W, Angielski S. Effect of (ÿ)-
hydroxycirate on the activities of ATP citrate lyase and the
enzymes of acetyl-CoA metabolism in rat brain. Acta Biochim
Pol 1976; 23: 227±234.
20 McCarty MF. Promotion of hepatic lipid oxidation and gluconeo-
genesis as a strategy for appetite control. Med Hypotheses 1994; 42:
21 McGarry JD, Foster DW. In support of the roles of malonyl-CoA
and carnitine acyltransferase I in the regulation of hepatic fatty
acid oxidation and ketogenesis. J Biol Chem 1979; 254: 8163±
22 Hellerstein MK, Xie Y. The indirect pathway of hepatic glycogen
synthesis and reduction of food intake by metabolic inhibitors.
Life Sci 1993; 53: 1833±1845.
23 Badmaev V, Majeed M, Conte AA. Garcinia cambogia for weight
loss. [Letter]. JAMA 1999; 282: 233±234.
24 Firenzuoli F, Gori L. Garcinia cambogia for weight loss. [Letter].
JAMA 1999; 282: 234.
25 Heyms®eld SB, Allison DB, Vasselli JR, Pietrobelli A, Green®eld D,
Nunez C. Garcinia cambogia for weight loss. [Letter]. JAMA 1999;
282: 234±235.
26 Schaller JL. Garcinia cambogia for weight loss. [Letter]. JAMA
1999; 282: 234.
27 Badmaev V, Majeed M. Open ®eld, physician controlled, clinical
evaluation of botanical weight loss formula citrin. Presented at:
Nutracon 1995: Nutraceuticals, Dietary Supplements and Functional
Foods, Las Vegas, NV, 11±13 July, 1995.
28 Conte AA. A non-prescription alternative in weight reduction
therapy. Am J Bariatr Med 1993; Summer: 17±19.
29 Girola M, de Bernardi M, Contos S, Tripodi S, Ventura P,
Guarino C, Marletta M. Dose effect in lipid-lowering activity of
a new dietary integrator (chitosan, Garcinia cambogia extract and
chrome). Acta Toxicol Ther 1996; 17: 25±40.
30 Thom E, Andrews B. Short- and long-term ef®cacy and
tolerability of (ÿ)-hydroxycitrate in the treatment of
obesity. [Abstract]. Int J Obes Relat Metab Disord 1997; 21(Suppl
2): S53.
31 Westerterp-Plantenga MS, Kovacs EMR. The paradoxical effect of
(ÿ)-hydroxycitrate on energy intake regulation in humans.
[Abstract]. Int J Obes Relat Metab Disord 2000; 24(Suppl 1): S189.
32 Heyms®eld SB, Allison DB, Vasselli, JR, Pietrobelli A, Green®eld D,
Nunez C. Garcinia cambogia (hydroxycitric acid) as a potent
antiobesity agent. JAMA 1998; 280: 1596±1600.
33 Kriketos AD, Thompson HR, Greene H, Hill JO. (ÿ)-Hydroxycitric
acid does not affect energy expenditure and substrate oxidation
in adult males in a post-absorptive state. Int J Obes Relat Metab
Disord 1999; 23: 867±873.
34 Loon L van, Rooijen JJM van, Niesen B, Verhagen H, Saris WHM,
Wagenmakers AJM. Effects of (ÿ)-hydroxycitrate supplementa-
tion on substrate metabolism at rest and during exercise in
humans. Am J Clin Nutr 2000; 72: 1445±1450.
35 Rothacker DQ, Waitmann BE. Effectiveness of Garcinia cambogia
and natural caffeine combination in weight loss Ð a double-blind
placebo-controlled pilot study. [Abstract]. Int J Obes Relat Metab
Disord 1997; 21(Suppl 2): S53.
36 Kovacs EMR, Westerterp-Plantenga MS, de Vries M, Brouns F,
Saris WHM. The effect of chronic ingestion of (ÿ)-hydroxycitrate
and (ÿ)-hydroxycitrate combined with medium-chain triglycer-
ides on satiety (submitted).
37 Bach AC, Babayan VK. Medium-chain triglycerides: an update.
Am J Clin Nutr 1982; 36: 950±962.
38 Beckers EJ, Jeukendrup AE, Brouns F, Wagenmakers AJM,
Saris WHM. Gastric emptying of carbohydrate Ð medium
chain triglyceride solutions in rest. Int J Sports Med 1992; 13:
39 Bremer J. Carnitine Ð metabolism and functions. Physiol Rev
1983; 63: 1420±1479.
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 7
40 Hill JO, Peters JC, Yang D, Shart T, Kaler M, Abumrad NN,
Greene HL. Thermogenesis in humans during overfeeding with
medium-chain and long-chain triglycerides. Am J Clin Nutr 1991;
53: 1130±1133.
41 Wymelbeke V van, Himaya A, Louis-Sylvestre J, Fantino M.
In¯uence of medium-chain and long-chain triacylglycerols on
the control of food intake in men. Am J Clin Nutr 1998; 68:
42 Bach AC, Ingenbleek Y, Frey A. The usefulness of dietary medium-
chain triglycerides in body weight control: fact or fancy? J Lipid
Res 1996; 37: 708±726.
43 Schoeller DA, Santen E v, Peterson DW, Diez W, Jaspan J, Klein
PD. Total body water measurement in humans with
labeled water. Am J Clin Nutr 1980; 33: 2686±2693.
44 Siri, WE. Body composition from ¯uid spaces and density: ana-
lysis of methods. In: Brozek J, Henschel A (eds). Techniques for
measuring body composition. National Academy of Science:
Washington, DC; 1961. pp 223±244.
45 Marken Lichtenbelt WD van, Westerterp KR, Wouters L. Deuter-
ium dilution as a method for determining total body water: effect
of test protocol and sampling time. Br J Nutr 1994; 72: 491±497.
46 Stunkard AJ, Messick S. The three-factor eating questionnaire to
measure dietary restraint, disinhibition, and hunger. J Psychosom
Res 1985; 29: 71±83.
47 Westerterp-Plantenga MS, Rolland V, Wilson SAJ, Westerterp KR.
Satiety related to 24 h diet-induced thermogenesis during high
protein=carbohydrate vs high fat diets measured in a respiration
chamber. Eur J Clin Nutr 1999; 53: 1±8.
48 Herman CP, Polivy J. Restrained eating. In: Stunkard AJ (ed).
Obesity. W.B. Saunders: Philadelphia, PA; 1980. pp 208±225.
49 Moore JJ, Marcus M, Sax SM. Kinetic assay of b-hydroxybutyrate
in plasma with cobas bio centrifugal analyzer. Clin Chem 1982;
73: 1334±1339.
50 Stichting Nederlands Voedingsstoffenbestand. Nevo tabel. Voor-
lichtingsbureau voor de voeding: Den Haag; 1996.
51 Harris JA, Benedict FG. A biometric study of basal metabolism in
man. Carnegie Institution: Washington, DC; 1919.
52 Lorr M, McNair DM. Manual. Pro®le of mood states. Bi-polar form
(POMS-BI). Educational and Industrial Testing Service (EDITS):
San Diego, CA; 1984.
53 Schoffelen PFM, Westerterp KR, Saris WHM, ten Hoor F. A dual
respiration chamber with automated calibration. J Appl Physiol
1997; 83: 2064±2072.
54 Schrauwen P, Marken Lichtenbelt van WD, Saris WHM,
Westerterp KR. Changes in nutrient oxidation in response to a
high-fat diet. Am J Clin Nutr 1997; 66: 276±282.
55 Weir JBDV. New methods for calculating metabolic rate
with special references to protein metabolism. J Physiol 1949;
109: 1±9.
56 Westerterp KR, Wilson SAJ, Rolland V. Diet induced thermo-
genesis measured over 24 h in arespiration chamber:
effect of diet composition. Int J Obes Relat Metab Disord 1998;
22: 1±6.
57 Brouwer E. On simple formulae for calculating the heat expen-
diture and the quantities of carbohydrate and fat oxidised in
metabolism of men and animals, from gaseous exchange (oxygen
intake and carbonic output) and urine-n. Acta Physiol Pharmac
Neerlandica 1957; 6: 795±802.
58 Greenwood MRC, Cleary MP, Gruen R, Blase
D, Stern JS, Triscari
J, Sullivan AC. Effect of (ÿ)-hydroxycitrate on development of
obesity in the Zucker obese rat. Am J Physiol 1981; 240: E72±
59 Sullivan AC, Triscari J, Hamilton JG, Miller ON, Wheatley VR.
Effect of (ÿ)-hydroxycitrate upon the accumulation of lipid in
the rat. I Lipogenesis. Lipids 1974; 9: 121±129.
60 Dulloo AG, Fathi M, Mensi N, Girardier L. Twenty-four-hour
energy expenditure and urinary catecholamines of humans con-
suming low-to-moderate amounts of medium-chain triglycerides:
a dose-response study in a human respiratory chamber. Eur J Clin
Nutr 1996; 50: 152±158.
(ÿ)-Hydroxycitrate and energy expenditure
EMR Kovacs
et al
International Journal of Obesity
Page 8
  • Source
    • "All the above findings were in agreement with the most recent meta-analysis of RCTs which revealed that G. cambogia extract possessed limited or no effects on weightloss in human subjects [131]. Moreover, this study showed no effect on satiety or calorie intake in overweight individuals consuming their habitual diet, which is in agreement with past studies [41, 60, 75]. However, such comparisons must be made with caution as the variations in the formulations, doses administered, RCTs designs, and study populations might contribute to the discrepancy of the results. "
    [Show abstract] [Hide abstract] ABSTRACT: Garcinia is a plant under the family of Clusiaceae that is commonly used as a flavouring agent. Various phytochemicals including flavonoids and organic acid have been identified in this plant. Among all types of organic acids, hydroxycitric acid or more specifically (-)-hydroxycitric acid has been identified as a potential supplement for weight management and as antiobesity agent. Various in vivo studies have contributed to the understanding of the anti-obesity effects of Garcinia/hydroxycitric acid via regulation of serotonin level and glucose uptake. Besides, it also helps to enhance fat oxidation while reducing de novo lipogenesis. However, results from clinical studies showed both negative and positive antiobesity effects of Garcinia/hydroxycitric acid. This review was prepared to summarise the update of chemical constituents, significance of in vivo/clinical anti-obesity effects, and the importance of the current market potential of Garcinia/hydroxycitric acid.
    Full-text · Article · Aug 2013 · Evidence-based Complementary and Alternative Medicine
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    • "? + 5 Kovacs et al. 2001 [26] "
    [Show abstract] [Hide abstract] ABSTRACT: The aim of this systematic review is to examine the efficacy of Garcinia extract, hydroxycitric acid (HCA) as a weight reduction agent, using data from randomised clinical trials (RCTs). Electronic and nonelectronic searches were conducted to identify relevant articles, with no restrictions in language or time. Two independent reviewers extracted the data and assessed the methodological quality of included studies. Twenty-three eligible trials were identified and twelve were included. Nine trials provided data suitable for statistical pooling. The meta-analysis revealed a small, statistically significant difference in weight loss favouring HCA over placebo (MD: -0.88 kg; 95% CI: -1.75, -0.00). Gastrointestinal adverse events were twice as common in the HCA group compared with placebo in one included study. It is concluded that the RCTs suggest that Garcinia extracts/HCA can cause short-term weight loss. The magnitude of the effect is small, and the clinical relevance is uncertain. Future trials should be more rigorous and better reported.
    Full-text · Article · Jan 2011 · Journal of obesity
  • Source
    • "MUFA vs. PUFA) have also been suggested to influence satiety. However, where effects have been shown, they have generally been small or occur only on extreme diets (Stubbs & Harbron 1996; van Wymelbeke et al. 1998; French et al. 2000; Lawton et al. 2000; Krotkiewski 2001 ) and some studies have failed to demonstrate an effect (Kamphuis et al. 2001; Kovacs et al. 2001; Bendixen et al. 2002; Alfenas & Mattes 2003; Flint et al. 2003; MacIntosh et al. 2003). "
    [Show abstract] [Hide abstract] ABSTRACT: Summary1Introduction2Physiological mechanisms of satiation and satiety2.1 Physiological mechanisms of satiation2.1.1 Gastric mechanisms of satiation2.1.2 Intestinal mechanisms of satiation2.2 Physiological mechanisms of satiety2.2.1 Gut hormones – episodic signals of satiety2.2.2 Tonic satiety signals2.3 The integration of satiety signals in the brain2.3.1 Anorexigenic pathways in the hypothalamus2.3.2 Orexigenic pathways in the hypothalamus2.3.3 Other areas of the brain involved in satiation and satiety2.3.4 Reward pathways3Measuring satiation and satiety3.1 Measuring satiation3.2 Measuring satiety3.2.1 Free living vs. laboratory studies3.2.2 Preload studies3.2.3 Self-reported measures of satiety3.2.4 Measuring food intake3.2.5 Quantifying satiety3.3 Confounders in satiety research3.3.1 Physiological confounders3.3.2 Behavioural confounders4The effects of foods and drinks on satiety4.1 Protein and satiety4.2 Carbohydrates and satiety4.3 Fibre and satiety4.4 Intense sweeteners and satiety4.5 Fat and satiety4.6 Liquids and satiety4.7 Alcohol and satiety4.8 Energy density and satiety5The effect of external factors on satiation and satiety5.1 Palatability5.2 Variety5.3 Portion size5.4 Sleep5.5 Physical activity5.6 Television viewing and other distractions5.7 Social situations6Satiation, satiety and weight control6.1 Obesity genes and satiety6.2 Physiological differences in satiation and satiety responses in obese people6.3 Behavioural differences in the response to satiation and satiety in obesity7Conclusions SummaryIn the context of the rising prevalence of obesity around the world, it is vital to understand how energy balance and bodyweight are controlled. The ability to balance energy intake and expenditure is critical to survival, and sophisticated physiological mechanisms have developed in order to do this, including the control of appetite. Satiation and satiety are part of the body's appetite control system and are involved in limiting energy intake. Satiation is the process that causes one to stop eating; satiety is the feeling of fullness that persists after eating, suppressing further consumption, and both are important in determining total energy intake.Satiation and satiety are controlled by a cascade of factors that begin when a food or drink is consumed and continues as it enters the gastrointestinal tract and is digested and absorbed. Signals about the ingestion of energy feed into specific areas of the brain that are involved in the regulation of energy intake, in response to the sensory and cognitive perceptions of the food or drink consumed, and distension of the stomach. These signals are integrated by the brain, and satiation is stimulated. When nutrients reach the intestine and are absorbed, a number of hormonal signals that are again integrated in the brain to induce satiety are released. In addition to these episodic signals, satiety is also affected by fluctuations in hormones, such as leptin and insulin, which indicate the level of fat storage in the body.Satiation and satiety can be measured directly via food intake or indirectly via ratings of subjective sensations of appetite. The most common study design when measuring satiation or satiety over a short period is using a test preload in which the variables of interest are carefully controlled. This is followed by subjects rating aspects of their appetite sensations, such as fullness or hunger, at intervals and then, after a predetermined time interval, a test meal at which energy intake is measured. Longer-term studies may provide foods or drinks of known composition to be consumed ad libitum and use measures of energy intake and/or appetite ratings as indicators of satiety. The measurement of satiation and satiety is complicated by the fact that many factors besides these internal signals may influence appetite and energy intake, for example, physical factors such as bodyweight, age or gender, or behavioural factors such as diet or the influence of other people present. For this reason, the majority of studies on satiation and satiety take place in a laboratory, where confounders can be controlled as much as possible, and are, therefore, of short duration.It is possible for any food or drink to affect appetite, and so it is important to determine whether, for a given amount of energy, particular variables have the potential to enhance or reduce satiation or satiety. A great deal of research has been conducted to investigate the effect of different foods, drinks, food components and nutrients on satiety. Overall, the characteristic of a food or drink that appears to have the most impact on satiety is its energy density. That is the amount of energy it contains per unit weight (kJ/g, kcal/g). When energy density is controlled, the macronutrient composition of foods does not appear to have a major impact on satiety. In practice, high-fat foods tend to have a higher energy density than high-protein or high-carbohydrate foods, and foods with the highest water content tend to have the lowest energy density. Some studies have shown that energy from protein is more satiating than energy from carbohydrate or fat. In addition, certain types of fibre have been shown to enhance satiation and satiety. It has been suggested that energy from liquids is less satiating then energy from solids. However, evidence for this is inconsistent, and it may be the mode of consumption (i.e. whether the liquid is perceived to be a food or drink) that influences its effect on satiety. Alcohol appears to stimulate energy intake in the short-term, and consuming energy from alcohol does not appear to lead to a subsequent compensatory reduction in energy intake.The consumption of food and drink to provide energy is a voluntary behaviour, and, despite the existence of sophisticated physiological mechanisms to match intake to requirements, humans often eat when sated and sometimes refrain from eating when hungry. Thus, there are numerous influences on eating behaviour beyond satiation and satiety. These include: the portion size, appeal, palatability and variety of foods and drinks available; the physiological impact on the body of physical activity and sleep; and other external influences such as television viewing and the effect of social situations.Because satiation and satiety are key to controlling energy intake, inter-individual differences in the strength of these signals and responsiveness to their effects could affect risk of obesity. Such differences have been observed at a genetic, physiological and behavioural level and may be important to consider in strategies to prevent or treat obesity.Overall, it is clear that, although the processes of satiation and satiety have the potential to control energy intake, many individuals override the signals generated. Hence, in such people, satiation and satiety alone are not sufficient to prevent weight gain in the current obesogenic environment. Knowledge about foods, ingredients and dietary patterns that can enhance satiation and satiety is potentially useful for controlling bodyweight. However, this must be coupled with an understanding of the myriad of other factors that influence eating behaviour, in order to help people to control their energy intake.
    Preview · Article · May 2009 · Nutrition Bulletin
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