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Oral Stimulation Influences Postprandial
Triacylglycerol Concentrations in Humans: Nutrient
Specificity
Thomas J. Tittelbach PhDa & Richard D. Mattes MPH, PhD, RDa
a Purdue University, West Lafayette, Indiana
Published online: 21 Jun 2013.
To cite this article: Thomas J. Tittelbach PhD & Richard D. Mattes MPH, PhD, RD (2001) Oral Stimulation Influences
Postprandial Triacylglycerol Concentrations in Humans: Nutrient Specificity, Journal of the American College of Nutrition,
20:5, 485-493, DOI: 10.1080/07315724.2001.10719057
To link to this article: http://dx.doi.org/10.1080/07315724.2001.10719057
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Original Research
Oral Stimulation Influences Postprandial Triacylglycerol
Concentrations in Humans: Nutrient Specificity
Thomas J. Tittelbach, PhD, and Richard D. Mattes, MPH, PhD, RD
Purdue University, West Lafayette, Indiana
Key words: oral stimulation, triacylglycerol, dietary fat, postprandial period, human
Objective: To determined whether the nature of the lipid in an oral stimulus modifies postprandial
triacylglycerolemia.
Methods: Sixteen healthy adults (eight male, eight female) participated in six test sessions conducted
weekly. The test sessions were administered randomly after overnight fasts and included: ingestion of 50 grams
of butter in capsules (to avoid oral stimulation with lipids) and 500 mL of water in 15 minutes followed by oral
stimulation with one of the following foods on a cracker: butter, unsaturated fatty acid (UFA) margarine, jelly,
UFA margarine ϩ jelly, cracker alone or no oral stimulation. Sensory stimulation entailed masticating and
expectorating ϳ5.0 g samples of each stimulus every three minutes for 110 minutes. Blood was drawn
immediately after preload ingestion and at minutes 35, 85, 200, 320, and 440 post loading and analyzed for serum
triacylglycerol (TAG), insulin and glucose concentrations.
Results: Only the oral samples containing the UFA margarine led to significant elevations of serum TAG
concentration compared to baseline (p Ͻ 0.05). Maximum change of TAG concentrations were greater following
orosensory stimulation with UFA margarine compared to orosensory stimulation with butter, jelly or UFA
margarine ϩ jelly. No differences were observed relative to vehicle alone or no orosensory stimulation, but this
is due to lower nadir values for these treatments. Insulin and glucose concentrations were not different between
treatments.
Conclusion: Oral exposure specifically to an unsaturated dietary lipid augments the postprandial rise of
TAG, compared to baseline.
initiated by a sensory property of the foods [6,7,8]. Sham
INTRODUCTION
feeding (which provides sensory stimulation without ingestion)
Electrophysiological studies demonstrate that long-chain
cis-polyunsaturated fatty acids (PUFA) are effective taste stim-
uli in rats [1]. Behavioral studies suggest that rats select long-
chain fatty acids based, in part, on olfactory and/or gustatory
cues associated with the number and position of double bonds
[2]. Saturated fatty acids (SFA) are not effective stimuli. The
presence of a fatty acid transporter messenger RNA exclusively
expressed in lingual tissue provides further support for a gus-
tatory mechanism for lipid detection in rats [3].
a palatable meal several hours after ingestion of an retinal ester
oil emulsion leads to an immediate increase in plasma retinal
ester concentration suggesting an orosensory influence on lipid
absorption [9]. More recent work indicates the sensory cue is a
dietary fat. Oral exposure to lipid following ingestion of 50
grams of safflower oil in capsules leads to significantly higher
peak TAG concentrations and a more prolonged TAG elevation
compared to exposure with fat-replacers (e.g. passelli, simp-
lesse and olestra) or primarily carbohydrate (CHO) based foods
(e.g., potatoes, cracker) [6,7,8]. Whether oral stimulation with
UFA or SFA differentially modulates postprandial TAG con-
centrations has not been determined in humans. Previous hu-
man studies have used primarily SFA as the oral stimulus. This
In humans, consumption of low or high fat meals subse-
quent to the ingestion of a high fat meal elicits a significant
augmentation of postprandial peak triacylglycerol (TAG) con-
centration [4,5]. Accumulating evidence suggests this may be
Address reprint requests to: Thomas J. Tittelbach, Ph.D., Baltimore Veterans Affairs Medical Center, Geriatrics (18), 10 N. Greene Street, Baltimore, MD 21201-1524.
E-mail: ttittelb@grecc.umaryland.edu.
Journal of the American College of Nutrition, Vol. 20, No. 5, 485–493 (2001)
Published by the American College of Nutrition
485

Oral Lipid Exposure and Postprandial Lipemia
study assessed whether the postprandial elevation in TAG
concentration is influenced by the nature of the lipid in the oral
cavity.
to 28 kg/m2 and non-smokers. Their mean Ϯ SEM age was
23 Ϯ 0.7 years and BMI was 22.2 Ϯ 0.4 kg/m2. Study proce-
dures were approved by the Purdue University Committee on
the Use of Human Research Subjects.
The mechanism by which oral lipid exposure influences
postprandial TAG concentration is not known but likely in-
volves an influence on lipid absorption. Oral stimulation with-
out lipid loading does not elevate postprandial TAG concen-
tration [8]. While there is evidence that this effect is
differentially influenced by specific fatty acids in the oral
cavity, the importance of the nature of the lipids in the gut has
not been assessed. Previous controlled trials have used lipid
composed of primarily PUFA. It is well known that saturation
level modifies fatty acid absorption, but not whether oral stim-
ulation influences the process. This trial tested responses with
a primarily SFA gastrointestinal (GI) load. Further, questions
about the importance of the interaction between the types of
fatty acids used at both sites (i.e., oral and GI) have not been
addressed. It may be hypothesized that, based on the specificity
in responses to a given food throughout the GI tract, a greater
TAG response would occur for matched oral and GI stimuli
than mismatched samples. This study addressed this question
by matching a GI load of primarily SFA rich lipid with oral
stimuli composed of items rich in SFA, unsaturated fatty acid
(UFA) and/or CHO.
General Protocol
The study consisted of six randomized test sessions, iden-
tical in design but differing in the composition of the oral
stimulus. Each treatment session was separated by at least one
week. Subjects arrived in the laboratory between 0600 and
0700 hours after a 12-hour fast. On the day prior to each testing
session, subjects were instructed to maintain their customary
diet but abstain from alcohol and caffeinated beverages and
exercise. Each treatment session included measurement of rest-
ing respiratory gas exchange (presented elsewhere), ingestion
of 50 g powdered butter in 0.8 g capsules (to avoid oral
stimulation with lipid) and 500 mL of water within ϳ15 min-
utes, followed by a 110 minute period of intermittent oral
stimulation. Subsequent to the oral stimulation period, subjects
rested in a semi-supine position for an additional 330 minutes
during which continuous gas exchange measurements and
blood samples were collected.
Oral Stimuli
CHO added to an oral lipid load amplifies the excursion of
postprandial TAG [10,11,12,13,14]. Possible explanations for
this response include differential rates of gastric emptying,
stimulation of endogenous TAG synthesis or inhibition of TAG
clearance. Test meal palatability also may contribute to dis-
crepancies in postprandial triacylglycerolemia [15]. The role of
orosensory stimulation with CHO on postprandial triacylglyc-
erolemia was assessed in this study by contrasting the effects of
oral stimuli matched for palatability but varying in sweetness
and macronutrient composition.
Study of these issues is important because elevated post-
prandial TAG concentration is associated with a preponderance
of potentially atherogenic, small, dense low-density lipopro-
tein-cholesterol and decreased high density lipoprotein-choles-
terol particles [16,17,18,19,20]. Elevated postprandial TAG
concentration is an independent risk factor for coronary artery
disease [21,22,23]. The potential health impact is great because
consumption of a typical Western diet leads to a sustained
postprandial state [15] that may be enhanced by its orosensory
characteristics.
Oral stimulation was initiated at three minute intervals for
110 minutes. Stimulation entailed masticating the oral stimulus
for 10 seconds and expectorating. Each oral stimulus consisted
of 0.7 g of a cracker (Premium Fat Free Saltine Crackers,
Nabisco, Inc., East Hanover, NJ), as a vehicle, with one of the
following: butter, a rich source of saturated fatty acids (SFA;
Sweet Cream Salted Butter, Land O’Lakes, Inc., Arden Hills,
MN), unsaturated margarine (UFA; Lee Iacocca’s Olivio Veg-
etable Oil Spread, Nicola Corporation, Boston, MA), grape
jelly, a carbohydrate source (CHO; Welch’s, Concord, MA) or
unsaturated margarine plus jelly (UFA ϩ CHO). Control con-
ditions included vehicle alone (Veh) and no oral stimulation
(NO). Twenty-six stimulus portions were prepared fresh the
morning of testing and were served at room temperature. All
samples were pre-weighed and expectorated samples were col-
lected and weighted. In addition to aliquots of non-masticated
stimuli, all expectorated samples were lyophilized to determine
the amount of unaccounted (i.e. ingested and plate residual)
stimuli. The weight and nutrient composition of the oral stimuli
are presented in Table 1.
Hematology
MATERIALS AND METHODS
Immediately after ingestion of the butter capsules, but be-
fore the initiation of oral stimulation, an indwelling cannula
was inserted into an antecubital vein and the first blood sample
was drawn (time 0). The blood glucose concentration was
immediately assessed (SureStep; Lifescan, Milpitas, CA) to
confirm that participants complied with the overnight fast.
Subjects
Eight men and eight women were recruited through public
advertisements. They were required to be in good health, 18 to
35 years of age, not using medication except oral contracep-
tives, exercising Յ 3 days per week, body mass index (BMI) 19
486
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Oral Lipid Exposure and Postprandial Lipemia
Table 1. Oral Stimuli Characteristics
Treatment Condition1
SFA
UFA
CHO
UFA ϩ CHO
Veh
NO
Weight (g/sample)
5.2
35.0
0.0
0.0
3.7
2.3
1.2
1.1
0.1
5.2
31.5
0.6
0.0
2.6
0.3
2.1
1.4
0.6
4.7
12.8
3.2
0.0
0.0
0.0
0.0
0.0
0.0
4.7
19.2
1.9
0.0
1.1
0.1
0.9
0.6
0.3
0.7
2.8
0.6
0.0
0.0
0.0
0.0
0.0
0.0
—
—
—
—
—
—
—
—
—
Energy* (kcal/sample)
Carbohydrate (g/sample)
Protein (g/sample)
Lipid (g/sample)
Saturated fatty acids
Unsaturated fatty acids†
Monounsaturated fatty acids
Polyunsaturated fatty acids
1 Oral stimuli: SFA ϭ butter, UFA ϭ unsaturated margarine, CHO ϭ jelly, UFA ϩ CHO ϭ unsaturated margarine ϩ jelly, Veh ϭ vehicle alone, NO ϭ no oral stimulus.
* Energy and macronutrient composition obtained from package label.
† Unsaturated lipid values were obtained from the USDA Nutrient Database for Standard Reference, Release 13 [33], except for treatment UFA for which the values used
came from the package label.
Subsequent blood samples were drawn at minutes 35, 85, 200,
320, and 440. Serum samples were analyzed spectrophoto-
metrically for TAG and glucose using a automated sample
analyzer (Cobas Mira Plus; Roche Diagnostic Systems,
Branchburg, NJ). Serum insulin was analyzed by radioimmu-
noassay (kit 14K; Linco Research, St. Louis, MO).
oral stimulus presentation, were not significantly different from
each other and were averaged to provide a mean hedonic rating
during the oral stimulus period. The 9-point hedonic rating
scale yields ordinal level data so a Friedman test was used to
determine significant differences in hedonic ratings between
treatments. A Wilcoxon rank-order test was used for post hoc
comparisons. Bonferroni corrections were made when applica-
ble. Statistical procedures were performed with the SPSS soft-
ware package release 10.0.5 (SPSS Inc., Chicago, IL). The
criterion for statistical significance was set at p Ͻ 0.05.
Sensory Testing
Subjects rated selected sensory properties of the oral stimuli
after the first and last stimulus presentation on 9-point category
scales. Overall opinion, appearance, creaminess, and flavor
were rated on scales with end anchors of “extremely unpleas-
ant” and “extremely pleasant.” Taste qualities (sweetness, sour-
ness, bitterness, saltiness), fat level, and aftertaste were rated on
scales ranging from “extremely low” to “extremely high.”
Hunger was assessed immediately before and after ingestion
of the capsules, after the oral stimulation period and at the end
of treatment using a 10 cm visual analog scale. The questions
“how hungry do you feel right now?” “how full does your
stomach feel right now?” and “how nauseous are you right
now?” were anchored by “not (hungry, full, nauseous) at all” to
“as (hungry, full, nauseous) as I’ve ever felt.”
RESULTS
The range of baseline TAG concentrations was 0.58–2.20
mmol/L. No significant difference in serum TAG concentration
was observed immediately following lipid ingestion (used as
baseline) across treatments. The change of serum TAG con-
centration over time associated with each study treatment con-
dition is shown in Fig. 1. For all treatment conditions, except
the UFA, a significant decrease in TAG concentration occurred
at minute 35. At 85 minutes, exposure to SFA and NO pro-
duced TAG concentrations that remained significantly lower
than baseline. Following oral exposure to the UFA and the
UFA ϩ CHO stimulus, serum TAG concentrations were sig-
nificantly elevated over their baseline values at the 320 minute
time point. UFA, CHO and NO conditions produced TAG
concentrations that were significantly lower than baseline at the
440 minute time point. Thus, only the stimuli that contained
UFA produced postprandial TAG concentrations significantly
greater than their baseline. Rank-order tests indicated that dif-
ferences were robust: 13 of 16 subjects for the UFA condition
(p Ͻ 0.01) and 11 of 16 subjects for the UFA ϩ CHO
condition, with one tie (p Ͻ 0.05) had serum TAG concentra-
tions greater than baseline at 320 minutes. Pooled standard
Statistical Analysis
All results presented are expressed as mean Ϯ SEM. The
effects of oral stimulation on TAG concentration, insulin and
glucose concentration were assessed by repeated measures
analysis of variance (ANOVA). The within-subject factors
were the composition of the oral stimulus and time. To test if
the responses were robust, rank-order tests were conducted.
Maximum change of TAG concentration was determined by
measuring the nadir to peak TAG response. Area under the
curve (AUC) for changes in TAG concentration were computed
by the trapezoidal method. One-sample and paired-samples t
tests were conducted for post hoc comparisons where appro-
priate. The two hedonic ratings, given after the first and last
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
487

Oral Lipid Exposure and Postprandial Lipemia
Fig. 1. Mean change of serum TAG concentration from baseline. Letters indicate time points where TAG concentrations are significantly different
from baseline. The gastrointestinal lipid load was given immediately prior to the first blood collection (minute 0). Oral stimulation occurred from
minute 0 to 110. Oral stimuli: SFA ϭ butter, UFA ϭ unsaturated margarine, CHO ϭ jelly, UFA ϩ CHO ϭ unsaturated margarine ϩ jelly, Veh ϭ
vehicle and NO ϭ no oral stimulus.
error of the mean for change of postprandial TAG concentra-
tion was 16.2 mmol/L. Differences were not observed between
the conditions containing UFA and vehicle alone or no orosen-
sory stimulation.
There were significant differences in maximum change of
postprandial TAG concentration (F(5,75) ϭ 3.17, p ϭ 0.012)
(Fig. 2). The UFA condition produced a maximum change of
postprandial TAG concentration significantly greater than SFA,
Fig. 2. Mean Ϯ SEM maximum change of postprandial triacylglycerol concentration. Significant differences across treatments are indicated by
dissimilar letters at each time point.
488
VOL. 20, NO. 5

Oral Lipid Exposure and Postprandial Lipemia
CHO and UFA ϩ CHO conditions. No significant effects of
oral stimulation on peak TAG concentration or duration were
observed.
stimuli. Saltiness was significantly higher for the Veh com-
pared to CHO. The association between hedonic responses to
the oral stimuli and AUC values for change of TAG were not
significant for any condition.
Baseline insulin concentrations ranged from 50.4 Ϯ 5.5 to
75.2 Ϯ 9.1 pmol/L and were not significantly different. The
change of serum insulin concentration over time associated
with each study treatment condition is shown in Fig. 3. Serum
insulin concentrations were not different between treatments.
Baseline glucose concentration ranged from 3.8 to 5.7 mmol/L
and did not differ significantly between conditions. The glucose
concentration decreased significantly over time (F(4,60) ϭ
6.52, p ϭ 0.0001), but did not change differentially across
treatments. Mean blood glucose concentrations at 440 minutes
ranged from 4.5 to 4.7 mmol/L.
No differences in hedonic ratings of the stimuli were ob-
served. Mean Ϯ SEM values were 5.4 Ϯ 0.3, 5.1 Ϯ 0.2, 4.9 Ϯ
0.3 and 4.5 Ϯ 0.3 for overall opinion, appearance, creaminess
and flavor, respectively. There were significant differences in
perceived fat level (p Ͻ 0.001), sweetness (p Ͻ 0.001) and
saltiness (p Ͻ 0.01). The perceived fat level was significantly
lower with CHO and Veh conditions compared to the SFA,
UFA and UFA ϩ CHO conditions. Perceived sweetness was
significantly greater during treatments containing jelly (CHO
and UFA ϩ CHO) compared to SFA, UFA, Veh. Sweetness
was not significantly different between the two jelly containing
Ingestion of the capsules was well tolerated by the subjects.
Ratings for nausea were not significantly different between
treatments with a inter-treatment mean Ϯ SEM of 1.3 Ϯ 3.2,
1.9 Ϯ 0.4, 0.9 Ϯ 0.3 and 0.9 Ϯ 0.3 cm on a 10 cm scale for
nausea ratings before capsule ingestion (Ϫ15 min), after cap-
sule ingestion (0 min), after orosensory stimulation (110 min)
and at the end of the session (440 min), respectively. No
significant differences were observed between treatments for
hunger ratings at baseline. Hunger increased significantly over
time (F(7,91) ϭ 21.8, p ϭ 0.000) after capsule ingestion in a
similar pattern for all treatments, Fig. 4.
More expectorated sample was lost, expressed as absolute
weight, during the UFA ϩ CHO condition compared to SFA,
UFA, and Veh conditions (F(4,60) ϭ 8.6, p Ͻ 0.005). How-
ever, the amount not recovered was small. Values for sample
losses were 0.3 Ϯ 2.1 g (0.2 Ϯ 1.6%) Ϫ SFA, 0.5 Ϯ 1.6 g
(0.4 Ϯ 1.2%) Ϫ UFA, 5.1 Ϯ 2.6 g (4.2 Ϯ 2.1%) Ϫ CHO,
10.4 Ϯ 1.9 g (8.5 Ϯ 1.6%) Ϫ UFA ϩ CHO and 3.7 Ϯ 0.8 g
(27.0 Ϯ 4.4%) Ϫ Veh. The larger sample losses relative to total
weight for the Veh condition is attributed to the drier and more
viscous masticated material not entirely expectorated compared
Fig. 3. Mean change of serum insulin concentration from baseline. Letters indicate time points where insulin concentrations are significantly different
from baseline. The gastrointestinal lipid load was given immediately prior to the first blood collection (minute 0). Oral stimulation occurred from
minute 0 to 110. Oral stimuli: SFA ϭ butter, UFA ϭ unsaturated margarine, CHO ϭ jelly, UFA ϩ CHO ϭ unsaturated margarine ϩ jelly, Veh ϭ
vehicle, and NO ϭ no oral stimulus.
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
489

Oral Lipid Exposure and Postprandial Lipemia
Fig. 4. Hunger ratings were assessed using a 10 cm visual analog scale at Ϫ15 (before capsule ingestion), 0 (after capsule ingestion), 110 (after
orosensory stimulation) and at 440 (end of session) minutes. Subjects were asked “how hungry do you feel right now?”. Oral stimulation occurred
from minute 0 to 110. Oral stimuli: SFA ϭ butter, UFA ϭ unsaturated margarine, CHO ϭ jelly, UFA ϩ CHO ϭ unsaturated margarine ϩ jelly,
Veh ϭ vehicle and NO ϭ no oral stimulus.
to the much less viscous, almost watery, consistency of the oral
stimuli containing the butter, margarine or jelly. Factoring in
residue left on the serving plates and percentage of lipid per
sample, the amount of lipid possibly ingested equaled 1.9 g for
the UFA ϩ CHO condition. Loss of oral stimulus from the
UFA condition was not significantly different from the other
treatments.
relationship between free fatty acid saturation and the rapidity
and potency of effect on the Kϩ current. Tsuruta et al. [2] found
that rats select long-chain PUFA (including mono-UFA) from
gustatory and/or olfactory cues. Whether these mechanisms for
lipid detection occur in humans has yet to be determined, but
preliminary evidence from prior work and this study support a
gustatory component for dietary lipids [8]. The present finding
of a significant rise only with the UFA stimuli is consistent
with the reported fatty acid specificity noted in rats [1].
Although the relative increase in postprandial TAG concen-
tration was small (0.29 and 0.16 mmol/L 320 minutes post-
loading compared to baseline for UFA and UFA ϩ CHO,
respectively), it cannot be dismissed as inconsequential. Dubois
et al. [25] have shown that relatively small changes in post-
prandial triacylglycerolemia (0.21 mmol/L) are capable of al-
tering the composition and concentration of high-density li-
poproteins and low-density lipoproteins. The peak and duration
of the postprandial TAG response between oral stimuli were
not significantly different, due in large part to the large inter-
individual variation which is characteristic of human postpran-
dial responses [26]. TAG concentrations expressed as maxi-
mum change were significantly greater during UFA compared
to SFA, CHO and UFA ϩ CHO conditions, but were similar to
Veh and NO conditions. Maximum TAG concentrations are
determined by taking the mean difference from nadir to peak
TAG concentration. The similarity in maximum change of
TAG concentration values for UFA and control conditions
occurred because the nadir TAG concentrations were lower for
DISCUSSION
A significant increase of postprandial TAG concentrations
occurred only when the oral stimulus contained the UFA, when
compared to baseline. The predominantly SFA stimulus (but-
ter), CHO stimuli (jelly and cracker) and the no oral stimulus
control did not promote increased TAG concentrations at any
time postprandially. The oral stimuli were not ingested, sug-
gesting the UFA effect was attributable to its orosensory stim-
ulation. The UFA and UFA ϩ CHO oral stimuli contained a
six- and threefold greater quantity, respectively, of PUFA com-
pared to SFA, CHO, Veh and NO conditions. The most parsi-
monious explanation for the observed differential responses is
provided by rat studies that indicate selected lipids are detected
in the oral cavity via a gustatory mechanism [1,24,2]. Gilbert-
son et al. [1] have shown that long-chain cis-PUFA inhibit
delayed-rectifying Kϩ channels in taste receptor cells. SFA
have no significant effect in rats. Although not significantly
different, Gilbertson et al. [1] reported a trend for an indirect
490
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Oral Lipid Exposure and Postprandial Lipemia
the Veh (Ϫ0.33 mmol/L) and NO (Ϫ0.34 mmol/L) conditions
relative to the SFA, CHO and UFA ϩ CHO conditions (Ϫ0.27,
Ϫ0.29, and Ϫ0.29 mmol/L, respectively). This produced a
larger maximum change of TAG concentration for the Veh and
NO conditions, even though their peak TAG concentrations
were only 0.11 and 0.05 mmol/L, respectively, compared to the
UFA peak TAG concentration of 0.29 mmol/L.
linoleic acid and 10% linolenic acid). This study used capsules
of powdered butter which contained approximately 62% satu-
rated fatty acid [33]. 13C-labelled fatty acid tracer studies have
determined that absorption of saturated fatty acids are poor
(78%) in comparison to the almost complete absorption of
unsaturated fatty acids (99.9%) [34,35,36]. Butterfat contains
primarily long-chain SFA (myristic, palmitic and stearic acids)
[37]. In rats, butterfat absorption is 55% lower than safflower
oil [38]. Thus, the lower absolute level of response between this
study and previous work in humans may be due to poor
absorption of the GI load. In fact, the change of TAG concen-
tration was significantly lower than baseline at 35 minutes in
this study using butter as the GI load compared to similar
studies using safflower oil, where the 35 minute TAG concen-
tration was not different from baseline [7,8]. It is also plausible
that the differences are due to varying rates of TAG clearance,
as the degree of saturation and fatty acid chain length may
affect lipoprotein lipase activity [39,40].
Textural properties of dietary lipids are regarded as the
primary cue for their discrimination [27]. Electrophysiological
tests in rhesus macaques indicate that texture alone is a suffi-
cient stimulus as paraffin and silicone (chemically different
from dietary lipids, but with similar textural properties) are
effective stimuli [28]. However, it is unlikely the response
observed here is attributable to the textural properties of the
oral lipid stimuli since discrepant TAG concentrations were
observed between oral stimuli comparable in texture (SFA and
UFA). Other studies have also failed to note differential re-
sponses to stimuli closely matched on texture [6,7]. Further
support for a non-textural oral cue is provided by Mela et al.
[29], who demonstrated that solutions of PUFA are rated higher
in fat compared to SFA solutions when matched for texture. In
the present study, palatability can not account for these differ-
ences as subjects rated the oral stimuli equally palatable. Cog-
nitive influences can not be ruled out as subjects discriminated
between the oral stimuli, and cognitive cues have been shown
to influence several cephalic phase responses in humans
[30,31]. However, a previous human study using fat-free and
fat-containing versions of the same food, closely matched on
sensory properties, led to discrepant TAG responses [6]. Thus
a cognitive influence is not necessary for the effect.
There was no effect of oral stimulation with the CHO
stimuli on the postprandial TAG concentration. This lack of
response is in agreement with a previous study, indicating that
sweetness alone is not responsible for the elevation in post-
prandial triacylglycerolemia in humans [41]. An effect of oral
stimulation with the UFA ϩ CHO condition on postprandial
TAG concentration was observed. However, the response is
likely due to the effects imparted by the UFA margarine rather
than the jelly as the oral stimulus containing only jelly had no
effect.
We did not measure TAG-rich lipoprotein fractions. Abia et
al. [42] has shown that two oils similar in mono-UFA compo-
sition produced equal TAG plasma concentrations, but different
TAG-rich lipoprotein responses, during the postprandial pe-
riod, suggesting that determination of postprandial total TAG
concentrations can be misleading when assessing the health
implications of postprandial triacylglycerolemia. Thus, the
health implications of this phenomenon warrant further char-
acterization.
Previous human studies investigating the effect of oral lipid
stimulation on postprandial TAG have used an oral stimulus
and GI load that were not matched for nutrient composition
[32,6,7,8]. In particular, the effective oral stimulus in previous
studies was butter or cream cheese (sources of primarily SFA),
while the GI load contained capsules composed entirely of
safflower oil (source of primarily PUFA) [6,7,8]. The present
study used butter as the oral stimulus and capsules of butter for
the GI load. Based on a hypothesis of specificity in responses
to a given food throughout the gastrointestinal tract, a greater
TAG response was expected for matched oral and GI stimuli
than mismatched samples. However, the postprandial TAG
concentrations to matched stimuli were no different from NO
stimulation or Veh treatments and were lower than responses to
the mismatched pair of UFA (oral) and SFA (GI). Given the
stronger effect of UFA oral stimuli, the possibility of a greater
postprandial TAG response for a UFA oral and GI pairing
warrants evaluation.
CONCLUSION
These data add to a growing body of evidence indicating
that lipid is detected in the oral cavity and alters postprandial
triacylglycerolemia. Consistent with electrophysiological data
in rats, these finding indicate UFA may be especially effective
oral stimuli. The effect of oral stimulation on postprandial TAG
concentration may be greatest if the oral stimulus and GI lipid
load are both UFA, possibly due to its stronger gustatory effect
and more efficient absorption. Given the association between
postprandial TAG concentration and atherogenesis, continued
study of this issue is warranted.
The smaller postprandial TAG response observed here com-
pared to previous studies [6,7,8] may be due to differences in
the GI load used. The gastric load used in previous studies
contained primarily PUFA (safflower oil is approximately 70%
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Oral Lipid Exposure and Postprandial Lipemia
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ACKNOWLEDGEMENT
17. Austin MA: Plasma triglyceride as a risk factor for coronary heart
disease. The epidemiologic evidence and beyond. Am J Epidemiol
129:249–259, 1989.
The authors would like to thank Dana Wislocki for her
assistance in the conduct of this study.
18. Groot PH, van Stiphout WA, Krauss XH, Jansen H, van Tol A, van
Ramshorst E, Chin-On S, Hofman A, Cresswell SR, Havekes L:
Postprandial lipoprotein metabolism in normolipidemic men with
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Received March 19, 2001; revision accepted August 9, 2001.
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