The Journal of Nutrition

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Slowly and Rapidly Digested Fat Emulsions

Are Equally Satiating but Their Triglycerides
Are Differentially Absorbed and Metabolized
in Humans1,2
Jennifer B. Keogh,3,7 Tim J. Wooster,4 Matthew Golding,4,8 Li Day,4 Bärbel Otto,5
and Peter M. Clifton3,6,9*

Downloaded from jn.nutrition.org at UNIVERSIDAD DE CHILE MEDICINA - SISIB on March 27, 2012
3
Commonwealth Scientific and Industrial Research Organization Preventative Health Flagship, Commonwealth Scientific and Industrial
Research Organization Food and Nutritional Sciences, Adelaide 5000, South Australia, Australia; 4Commonwealth Scientific and
Industrial Research Organization Food Futures Flagship, Commonwealth Scientific and Industrial Research Organization Food and
Nutritional Sciences, Werribee VIC 3030, Australia; 5Medizinsche Klinik-Innenstadt, Klinikum der Universität, Munich D-80366,
Germany; and 6Clinical Centre for Research Excellence in Nutritional Physiology, University of Adelaide, Adelaide 5000, South
Australia, Australia

Abstract
Little is known about the effect of dietary fat emulsion microstructure on plasma TG concentrations, satiety hormones,
and food intake. The aim of this study was to structure dietary fat to slow digestion and flatten postprandial plasma TG
concentrations but not increase food intake. Emulsions were stabilized by egg lecithin (control), sodium sterol lactylate, or
sodium caseinate/monoglyceride (CasMag) with either liquid oil or a liquid oil/solid fat mixture. In a randomized, double-
blind, crossover design, 4 emulsions containing 30 g of fat in a 350-mL preload were consumed by 10 men and 10 women
(BMI = 25.1 6 2.8 kg/m2; age = 58.8 6 4.8 y). Pre- and postprandial plasma TG, cholecystokinin (CCK), glucagon-like
peptide-1 (GLP-1), and peptide YY (PYY) concentrations and food intake were measured. In a second experiment in a
subset of the participants (n = 8, 4 men and 4 women), 13C-labeled mixed TG was incorporated into 2 different emulsions
and breath 13C was measured over 6 h. In the first experiment, the postprandial rise in plasma TG concentrations following
the CasMag-stabilized emulsion containing 30% solid fat was lower than all other emulsions at 90 and 120 min (P , 0.05).
Plasma CCK (P , 0.0001), GLP-1 (P , 0.01), and PYY (P , 0.001) concentrations were also reduced following this
emulsion compared with control. Food intake at a test meal, eaten 3 h after the preload, did not differ among the
emulsions. In the second experiment, when measured by the 13C breath test, 25% of the TG in the CasMag emulsion was
absorbed and metabolized compared with control. In conclusion, fat can be structured to decrease its effect on plasma TG
concentrations without increasing food intake. J. Nutr. 141: 809–815, 2011.

Introduction
There is emerging interest in how the behavior of food structures,
especially emulsion systems, during digestion can influence the
body’s satiety mechanisms (1). The physiological responses to
food materials appear to be dependent not only on the macro-
nutrient composition and energy content but also on the way
components are assembled, i.e. the microstructure (2). The
1
Supported by the National Centre of Excellence for Functional Foods, Australia.
2
Author disclosures: J. B. Keogh, T. J. Wooster, M. Golding, L. Day, B. Otto, and
P. M. Clifton, no conflicts of interest.
7
Present address: Sansom Institute for Health Research, Division of Health
Sciences, University of South Australia, Adelaide SA 5000.
8
Present address: Institute of Food, Nutrition and Human Health, Massey
University, private bag 11 222, Palmerston North, New Zealand.
9
Present address: Baker IDI Heart and Diabetes Institute, GPO Box 664,
Adelaide, South Australia. 5001.
* To whom correspondence should be addressed. E-mail: peter.clifton@bakeridi.
edu.au.
assembly of food components into microstructures dictates both
the textural and sensory properties and the digestion of the food
products (3).
The digestion of fat plays a role in satiation and subsequent
energy regulation (4,5). Intraduodenal fat/fatty acids act as a
short-term control on food intake via negative feedback path-
ways that modulate gastrointestinal motility through the duo-
denal and ileal break mechanisms (6). The release of fatty acids
in the duodenum stimulates cholecystokinin (CCK)10 secretion,
which then slows gastric emptying by suppressing the muscular
contractions of the antrum and enhancing contractions of the
10
Abbreviations used: CasMag, caseinate/monoglyceride; CCK, cholecystoki-
nin; CSIRO, Commonwealth Scientific and Industrial Research Organization;
GLP-1, glucagon-like peptide-1; PYY, peptide YY; SSL–LO, sodium stearoyl
lactylate (liquid oil); SSL-LO/SF, sodium stearoyl lactylate (mixture of liquid oil and
solid fat).

ã 2011 American Society for Nutrition.

Manuscript received August 24, 2010. Initial review completed November 20, 2010. Revision accepted February 04, 2011. 809
First published online March 16, 2011; doi:10.3945/jn.110.131110.
pylorus (3,4). It is apparent that different rates of fatty acid
release have the potential to affect the pathways associated with
satiety/satiation and energy intake. The ability to understand,
and potentially influence, fat digestion through emulsion design
might then be a complementary measure to aid the regulation of
dietary intake. Fat droplet size controls available surface area for
lipase activity and thus has an impact on the rate of fat lipolysis
during digestion. This might have an effect on the degree of
satiety experienced after consuming food (7–9) and, if lipolysis
is slowed, may potentially prolong the intermeal interval by
producing a more persistent, but lower elevation of satiety
hormones.
Postprandial hyperlipidemia is a risk factor for atherothrom-
bosis with many potential mechanisms linking the two (10,11).
Strategies that decrease the magnitude and duration of post-
prandial lipemia may reduce the progression of atherosclerosis
and acute clinical events.
Our aim in this study was to explore the effects of emulsions
with fast and slow lipolysis rates in vivo on postprandial TG,
satiety hormones, and subsequent food intake. We hypothesized
that there would be persistent elevations of satiety hormones 3 h
following the slowly lipolyzed emulsion and food intake would
be reduced at a subsequent test meal.
Methods
Participants. In the first study, 10 men and 10 postmenopausal women
were recruited from the Commonwealth Scientific and Industrial
Research Organization (CSIRO) Human Nutrition volunteer database
in Adelaide, Australia. Inclusion criteria were age 20–65 y, BMI , 27kg/m2,
no recent history (past 3 mo) of weight loss or changes to diet or physical
activity routine, and a score of ,10 on the eating restraint section of the
validated Three Factor Eating questionnaire (12). A subset of 8 of these
individuals was studied in a second study.
Exclusion criteria were type 1 or 2 diabetes, self-reported liver and
kidney disease from a medical questionnaire, current gastrointestinal
disease, past history of gastrointestinal surgery (which could affect study
outcomes), and intolerance to fat or medications that affect gastrointestinal
motility, hunger, or appetite.
The study was approved by the Human Research Ethics Committee of
the CSIRO and participants provided written informed consent.
Structured emulsions. The 4 emulsion systems participants consumed
were designed to contain 30 g of fat in a 350-mL preload. Ivelip
emulsions (control) were purchased from Baxter Healthcare as a 20%
solution and were diluted to the required fat content with artificially
flavored/sweetened water. The other 3 emulsions were prepared using a
range of emulsifiers and solid/liquid fat combinations (Table 1). Small
amounts of food flavor, artificial sweetener, and color were added to the
emulsions to enhance their palatability. Briefly, all water-soluble ingre-
TABLE 1 Fat and emulsifier composition of test meals1
Name Emulsifier
Study 1
Control Egg lecithin (Ivelip)
SSL-LO Sodium sterol lactylate
SSL-LO/SF Sodium sterol lactyate
CasMag Sodium caseinate/monoglyceride
Study 2
Tween-80 Polyoxyethylene sorbitan monooleate (Tween-80)
CasMag Sodium caseinate/monoglyceride
1
In the case of Ivelip, the liquid oil was soybean oil; all other emulsions were prepared with canola oil.
810 Keogh et al.
dients were combined and mixed for at least 30 min at 658C to ensure
complete dissolution. The oil phase, and monoglyceride surfactant when
used, was then heated to 708C to ensure complete melting/dispersal. This
hot oil was then combined with the aqueous phase using a high-shear
Silverson mixer, which created a coarse emulsion with a mean particle
size of 10 mm. This coarse emulsion was then homogenized using a pilot
scale 2-stage Rannie homogenizer at a pressure of 35/10 MPa. The
homogenized emulsion was then pasteurized through an ultra high-
temperature plant at 708C for 30 s. The pasteurized emulsion was
aseptically filled into aluminum foil pouches (1.2 L/pouch) and kept
below ;48C until consumption.
The emulsion systems were designed to have the same sensory
properties during consumption, to be iso-viscous and iso-caloric, and to
have the same mean droplet size but to undergo different restructuring
within the gastric environment and thus to have different particle sizes
and lipolysis rates. The in vitro lipolysis rates are shown in Table 2.
Expt. 1 Protocol. This was a randomized crossover design of 4 test
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emulsions (20 weight% oil in water containing 30 g of fat). The Ivelip
emulsion, which served as the control, was liquid canola oil stabilized by
sodium stearoyl lactylate (SSL-LO), a mixture of liquid canola oil and
solid hydrogenated rapeseed oil stabilized by sodium stearoyl lactylate
(SSL-LO/SF), or a mixture of liquid canola oil and solid hydrogenated
rapeseed oil stabilized by a mixture of sodium caseinate and monoglyc-
eride surfactant (CasMag).
Participants attended the CSIRO outpatient clinic on 4 occasions
with 1 wk between treatments. They were provided with a standardized
meal to eat the night before each visit to control any effects of food
intake at the evening meal on the variables of interest. The meal
contained 3.3 MJ, 60 g protein, 65 g carbohydrate, and 30 g fat (11 g
saturated fat). Participants were asked to refrain from alcohol and
strenuous exercise for 24 h before visits and to fast for 12 h (water
permitted). Weight and height were measured (Mettler scales, model
AMZ14; A and D Mercury) in light clothing and BMI was calculated. A
canula was inserted into a forearm vein of participants on arrival.
Participants consumed 350 mL of the prepared preload containing 30 g
fat. The preloads were given in a randomized order and participants
were asked to consume them within 5 min. The preload was followed by
1500 mg paracetamol dissolved in 100 mL water for use as a measure of
gastric emptying (13). Subjective assessments of satiety were measured
on a 100-mm visual analogue scale (14) before and at 15, 30, 60, 90,
120, and 180 min after commencing the preload. Specific questions to
assess hunger and satiety were “How hungry do you feel?” and “How
satisfied do you feel?” Blood samples were taken at time 0 (fasting) and
at 15, 30, 60, 90, 120, and 180 min after the preload for analysis of
plasma TG, CCK, ghrelin, glucagon-like peptide-1 (GLP-1), and peptide
YY (PYY) concentrations.
Three hours after the preload, participants were offered a meal at
which each participant was provided with large servings of foods.
Instructions were given to eat until comfortably satisfied. The meal
consisted of either 800 g pasta with 800 g bolognaise sauce, 800 g veal
casserole with 800 g rice, or 800 g chicken curry with 800 g rice (7.0–7.3
MJ; 22–26% of energy as protein, 14–18% as fat, and 58–63% as
Fraction of fat phase as
Liquid oil Hydrogenated rapeseed oil
1
1
0.7 0.3
0.7 0.3
1
0.7 0.3
 TABLE 2 In vitro fatty acid release from various emulsions1

Initial rate, Fatty acid release, mmol

Emulsion mmol/min 30 min 60 min 120 min 180 min

Control (egg lecithin) 70 6 8a 222 6 7a 232 6 9a 244 6 11a 255 6 11a

SSL-LO (liquid oil) 23 6 3b 87 6 5.5b 106 6 9.2b 128 6 12b 143 6 13b
SSL-LO/SF (liquid and solid fat) 26 1c 50 6 2.2c 72 6 5.9c 100 6 5b 126 6 8b
CasMag (liquid and solid fat) 18 6 3b 92 6 5.1b 123 6 5.4b 167 6 11b 194 6 11b
1
Values are means 6 SEM, n = 4. Means in a column without a common letter differ, P , 0.05.

carbohydrate). Participants ate the same meal on each occasion to relationships among subjective measures of satiety, gut peptide concen-
control for energy density of the meals. Each food was weighed to the trations, and energy intake.
nearest gram before and after eating. Energy and nutrient composition
were calculated using Food Works 5.1 2007 (Xyris Software). This

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protocol was modified from one developed in an earlier study (15).
Results
Biochemical analyses. Aprotinin (500 MIU/L of blood; Trasylol;
Expt. 1. Ten men (BMI = 25.8 6 1.9 kg/m2, weight = 79.8 6
Bayer) was added to tubes for plasma CCK and ghrelin analysis and
dipeptidyl peptidase-IV inhibitor (10 mL/L blood; Linco) was added to 10.4 kg, age= 57.6 6 5 0.3 y) and 10 postmenopausal women
tubes for plasma GLP-1 analysis. Blood samples were stored on ice until (BMI = 24.3 6 3.4 kg/m2, weight = 66.9 6 12.2 kg, age = 59.4 6
processed and the plasma was isolated within 30 min of collection by 4.1 y) completed the study. No participants dropped out of the
centrifugation for 10 min at 2000 3 g and 58C (Allegra XR-12 Cen- experiment.
trifuge; Beckman Coulter). Aliquots were stored at 2808C. There was a main effect of time (P , 0.001), but not treatment,
Ghrelin, GLP-1, and PYY were measured in plasma using the and a significant time 3 treatment interaction on plasma TG
LINCOplex human gut hormone panel multiplex assay kit (LINCOplex concentrations (P , 0.001). Plasma TG concentrations after
human gut hormone panel HGT-68K, Millipore) according to the CasMag were lower (P , 0.05) compared with all other treatments
manufacturer’s instructions. Multianalyte profiling was performed on
at 90 and 120 min (Fig. 1). At 180 min, concentrations after
the Luminex-200 system and fluorescence data were analyzed by the
CasMag and SSL-LO/SF were lower than after the other 2 treat-
Liquichip analyzer software (version 1.0.5; Qiagen).
Plasma CCK concentrations were determined by a sensitive and ments and that after the control treatment was greater than after all
specific RIA, using an in-house method previously described by Riepl other treatments (all P , 0.05). There was an overall time (P ,
et al. (16). In short, the antibody (CH40IX), raised in rabbits, was 0.001) and treatment effect (P , 0.01) and a time 3 treatment
specifically directed to the biologically active site of CCK, including the interaction (P , 0.001) on plasma paracetamol concentrations
sulfated tyrosyl residue at position 7 from the C-terminal end, and (Fig. 2). Overall, concentrations after control, SSL-LO, and SSL-
showed no cross-reactivity with unsulfated CCK-8, unsulfated gastrin- LO/SF did not differ from one another, whereas those after CasMag
17, or unsulfated gastrin-34. The cross-reactivity to sulfated gastrin-17 were greater than after SSL-LO and SSL-LO/SF (P , 0.05) but did
was 1%. The mean minimal detectable concentration in extracted
plasma samples was 0.3 pmol/L. The intra-assay CV was 5.6% (at
0.7 pmol/L) and 7.2% (at 15.1 pmol/L).
Plasma TG concentrations were determined by GPO-PAP method kit
11488872 216 (Roche Diagnostics Australia) and control sera on a
Hitachi 902 automatic analyzer (Roche Diagnostics).
Plasma paracetamol concentrations were measured on a Hitachi 902
Automatic Analyzer using a Paracetamol (acetaminophen) Assay kit
(K8001, Cambridge Life Sciences).
All biochemical analyses were performed after study completion and
all samples for individuals were analyzed in the same assay on the same
day.

Expt. 2 protocol. A subset of the same participants (n = 8, 4 men and

4 women) attended the clinic on 2 occasions. They consumed a-350 mL
emulsion preload containing 30 g of liquid fat (canola oil) emulsified
with either CasMag or polyoxyethylene sorbitan monooleate (Tween 80)
into which 250 mg of a mixed TG containing 13C (Wagner Analysen
Technik. Vertriebs) was incorporated (Table 1).
TG concentrations in whole blood were determined on a finger prick
blood sample using a Cardiocheck test strip (Polymer Technology
Systems) at baseline and hourly following consumption of the test meals.

Statistical analysis. Statistical analyses were carried out using SPSS

16.0 for WINDOWS. Repeated-measures ANOVA was used to assess the
effects of the treatment. Significance was set at P # 0.05. Data in the text
are means 6 SD. When a main treatment effect was significant, means
were compared using least significant differences tests. When the time 3
treatment interaction was significant, post hoc t tests were performed at
each time point. Pearson’s correlations were performed to examine
FIGURE 1 Plasma TG concentrations in men and women before
and for 3 h after the consumption of 30 g of fat in 4 emulsions. Data
are mean 6 SEM, n = 20. *Different from all other treatments at 90
and 120 min and from all except SSL-LO/SF at 180 min, P , 0.05.

Effects of emulsion structure on food intake 811

not differ from the control treatment. At 60 min, the plasma
paracetamol concentration after CasMag was greater than after the
other 3 treatments (P , 0.05) (Fig. 2). These data suggest that
gastric emptying of liquids was quicker after ingestion of CasMag.
There was a time (P , 0.001) and treatment effect (P ,
0.001) and a time 3 treatment interaction (P , 0.001) on
plasma CCK concentrations (Fig. 3A). Overall, concentrations
after control, SSL-LO, and SSL-LO/SF did not differ, whereas
that after CasMag was lower (P , 0.05). Plasma CCK con-
centrations after CasMag were lower than all other treatments
at 60 and 90 min (P , 0.05).
Plasma ghrelin concentrations did not differ after the 4 treat-
ments (data not shown).
There were time (P , 0.001) and treatment (P , 0.05) effects
and a time 3 treatment interaction for plasma GLP-1 concen-
trations (P , 0.01) (Fig. 3B). Overall, the concentration after
CasMag was lower than after the other 3 emulsions, which did

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not differ from one another (P , 0.05). Plasma GLP-1 concen-
trations after CasMag at 60 and 90 min were lower than after
the other 3 treatments except SSL-LO at 60 min (P , 0.01). At
120 min, the concentration after CasMag was lower than after
control and SSL-LO (P , 0.05) and at 180 min was lower than
after SSL-LO only (P , 0.05).
There was a time (P , 0.001) and treatment (P , 0.01) effect
and a time 3 treatment interaction on plasma PYY concentra-
tions (P , 0.001). At 60 min, the concentration after CasMag
was lower than after the control treatment (P , 0.05) and at 90,
120, and 180 min than after all treatments except SSL-LO at
90 min (P , 0.01) (Fig. 3C).
There were no differences in subjective measures of satiety
(Fig. 4A,B) or food intake (data not shown) between treatments.
There were no correlations among subjective measures of
satiety, gut peptide concentrations, and energy intake.

Expt. 2. Whole blood TG concentrations were lower after

CasMag compared with control (Tween-80) (P , 0.01) (Fig. 5).
There was no rise in blood TG concentrations over 4 h after the

FIGURE 3 Plasma CCK (A), GLP-1 (B), and PYY (C ) concentrations

in men and women before and for 3 h after the consumption of 30 g of
fat in 4 emulsions. Data are mean 6 SEM, n = 20. Main effects
without a common letter differ, P , 0.001. To convert ng/L to pmol/L,
1 divide by 3.3; to convert ng/L to pmol/L, divide by 3.9.

FIGURE 2 Plasma paracetamol concentrations in men and women
before and for 3 h after the consumption of 30 g of fat in 4 emulsions.
Data are mean 6 SEM, n = 20. Main effects without a common letter
differ, P , 0.01. To convert g/L to mmol/L, divide by 151.
812 Keogh et al.
CasMag emulsion in contrast to the rise after the control
(Tween-80) treatment (Fig. 5).
Breath 13C appearance was slower when incorporated into
CasMag compared with the control (Tween-80) (P , 0.05) (Fig.
 Downloaded from jn.nutrition.org at UNIVERSIDAD DE CHILE MEDICINA - SISIB on March 27, 2012
FIGURE 5 Whole blood TG concentrations in 4 men and 4 women
before and for 6 h after the consumption of 30 g of fat in 2 emulsions.
Data are mean 6 SEM, n = 8. *Treatments differed, P , 0.001.

The results with the CasMag emulsion are in striking contrast

to those found by Feinle et al. (17) using orlistat, a competitive
pancreatic lipase inhibitor. In those studies using intraduodenal-
infused fat, the presence of orlistat inhibited gastric relaxation,
which would lead to accelerated gastric emptying as in our
study, but there was also an almost complete suppression of
CCK release and an increase in hunger and decrease in fullness
that were not seen using the slowly digested CasMag emulsion.
In addition, the degree of TG reduction with orlistat after a large
fat load was only 5–10% over 2–4 h, whereas it was ;70% with
CasMag over 3 h, admittedly with a smaller fat load (18). Thus,
there seems to be a dissociation in effects between a 30%
inhibition of lipolysis and a reduced rate of lipolysis due to the

FIGURE 4 Hunger (A) and satiety (B) responses before and for 6 h
after the consumption of 30 g of fat in 4 emulsions in humans. Data
are mean 6 SEM, n = 20.

6) with the level at 180 min only ;25% of that seen with the
control (Tween-80).

Discussion
The main finding of the study was that altering fat structure by
inducing emulsion coalescence within the stomach has a pro-
found effect on plasma TG. The paracetamol gastric-emptying
studies suggest that lack of feedback from lipolysis products from
the CasMag-stabilized emulsion allows early rapid gastric emp-
tying of liquids for the first 90 min. Finally, the 13C studies show
that after 3 h, ,25% of the CasMag partially-coalesced emulsion
had been digested, absorbed, and metabolized to CO2 compared
with the small control emulsion droplets. Despite the reduced
energy absorption from the CasMag emulsion at 3 h and the FIGURE 6 Breath 13C in men and women before and for 6 h after
lower satiety hormone profile over the last 90 min, there was no the consumption of 30 g of fat in 2 emulsions. Data are mean 6 SEM,
negative impact on energy intake at a subsequent meal. n = 8. *Treatments differed, P , 0.01.

Effects of emulsion structure on food intake 813

formation of larger particles on plasma TG and CCK levels and
satiety. Preservation of the initial CCK response may well be
very important in maintaining fullness. The satiety hormones
appeared to rise at the same initial rate with all emulsions but to
decrease over time to different extents. The ghrelin response did
not differ between emulsions and this may be an important
factor in the lack of differences in hunger, fullness, and food
intake between emulsions. We found in previous studies that
ghrelin was an important predictor of food intake after protein
and glucose loads (19). The biphasic response in hormone levels
may be due to 2 populations of particles being present in the
CasMag emulsion: small, rapidly lipolyzed particles that stim-
ulate the initial CCK and GLP1 and larger, slowly lipolyzed
particles that do not maintain these levels.
Our results are similar to the findings on food intake by
Logan et al. (20) and Diepvens et al. (21). In the study by Logan,
there were two 3-wk periods during which 28 participants
consumed either yogurt with 5 g of a novel fat emulsion (Olibra)
postulated to be slowly digested or a control yogurt for breakfast
followed by an acute study assessing appetite and food intake.
No differences were found in food intake from the buffet meal,
for the remainder of the study day, or for the 6-wk study period.
In the study by Diepvens et al. (21), 21 young normal weight and
20 older overweight participants consumed yogurt with or
without a novel fat emulsion. The test yogurt reduced hunger
and the desire to eat and increased the time interval to the next
meal in the younger participants. There were no effects on
appetite scores in the older participants and no differences in
energy intake in the whole group. In contrast to these findings,
Burns et al. (22) observed lower energy intakes of ~1 MJ after a
test yogurt containing 5 g of this novel fat emulsion (Olibra)
compared with control yogurt. In a follow-up dose-response
study, Burns et al. (23) found that energy intakes were signi-
ficantly reduced by 2, 4, and 6 g of Olibra. In a longer term study
of weight loss maintenance, yogurt containing either Olibra or
placebo was given as a supplement for 18 wk after 6 wk of
weight loss (24). There was no significant increase in weight in
the Olibra group, whereas the placebo group gained weight. In
addition, the Olibra group was less hungry and had an increase
in GLP-1 concentrations after yogurt consumption at the end of
the study.
The delayed appearance of 13C in the breath in the current
study indicated that the digestion of fat was delayed. Similarly,
Haenni et al. (25) observed a longer orocecal transit time after
consumption of an emulsion based on palm and oat oil (Olibra),
indicating an effect on the ileal brake mechanism that is thought
to slow gastrointestinal transit time.
The flattened postprandial TG response should have an effect
on inflammatory markers such as IL-6, because a large fat load
($80 g) can double plasma levels (26), as well as increase TNFa
and the adhesion molecules vascular cell adhesion protein-1 and
inter-cellular adhesion molecule-1. A relationship was shown
between changes in serum TG concentrations and changes in
TNFa, IL-6, and vascular cell adhesion protein-1 concentrations
in normal participants and participants with type 2 diabetes
(27).
In the present study, a structured fat emulsion stabilized by
CasMag resulted in a profound reduction in plasma TG,
suggesting delayed lipolysis. This was confirmed by the much
slower appearance of breath 13C. Surprisingly, given the
relatively low absorption of fat from the CasMag emulsion,
there were no differences in measures of satiety or food intake.
The effects of fat structure on long-term food intake remain to be
further explored. Nevertheless, a fat emulsion that has a much
814 Keogh et al.
lower metabolic impact with no negative consequences of
increased food intake has great therapeutic potential, especially
in those with hypertriglyceridemia or metabolic syndrome.
Acknowledgments
We thank Jill Burnett, Rosemary McArthur, Lindy Lawson,
Ruth Pinches, Peter Royle, Julie Syrette, Anne McGuffin, and
Julia Weaver for contributions to the conduct of the clinical
trial. We thank Cathryn Seccafien, Candita Sullivan, and Mark
Mano for their technical expertise and Mi Xu for preparation of
the study material. We also thank Dr. Leif Lundin for
contribution to the initial discussions. J.B.K., T.J.W., M.G., L.D.,
and P.M.C. all contributed to aspects of the study design and
conduct and data analysis and interpretation; B.O. contributed
to data acquisition; J.B.K. and P.M.C. undertook the initial data
analyses; J.B.K. drafted the manuscript; T.J.W. and L.D.
critically reviewed the manuscript; and P.M.C. had primary
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responsibility for the final content. All authors read and
approved the final manuscript.
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