the chain length of dietary saturated fatty acids affects human postprandial lipemia
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The Chain Length of Dietary Saturated Fatty AcidsAffects Human Postprandial LipemiaTilakavati Karupaiah PhD, APD, ANa, Choon H Tan BSca, Karuthan Chinna PhDb & KalyanaSundram PhDc
a National University of Malaysia, Kuala Lumpur, MALAYSIA (T.K., C.H.T.),b University of Malaya, Kuala Lumpur, MALAYSIA (K.C.),c Malaysian Palm Oil Council, Kelana Jaya, Selangor, MALAYSIA (K.S.)Published online: 07 Jun 2013.
To cite this article: Tilakavati Karupaiah PhD, APD, AN, Choon H Tan BSc, Karuthan Chinna PhD & Kalyana Sundram PhD(2011) The Chain Length of Dietary Saturated Fatty Acids Affects Human Postprandial Lipemia, Journal of the AmericanCollege of Nutrition, 30:6, 511-521, DOI: 10.1080/07315724.2011.10719997
To link to this article: http://dx.doi.org/10.1080/07315724.2011.10719997
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Original Research
The Chain Length of Dietary Saturated Fatty AcidsAffects Human Postprandial Lipemia
Tilakavati Karupaiah, PhD, APD, AN, Choon H. Tan, BSc, Karuthan Chinna, PhD, Kalyana Sundram, PhD
National University of Malaysia, Kuala Lumpur, MALAYSIA (T.K., C.H.T.), University of Malaya, Kuala Lumpur, MALAYSIA
(K.C.), Malaysian Palm Oil Council, Kelana Jaya, Selangor, MALAYSIA (K.S.)
Key words: postprandial lipemia, dietary fat, saturated fatty acids, lipoproteins, TAG
Objective: Saturated fats increase total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) and
are linked to coronary artery disease risk. The effect of variance in chain length of saturated fatty acids (SFA) on
coronary artery disease in human postprandial lipemia is not well elucidated.
Methods: A total of 20 healthy volunteers were challenged with 3 test meals, similar in fat content (;31%
en) but varying in saturated SFA content and polyunsaturated/saturated fatty acid ratios (P/S). The 3 meals were
lauricþmyristic acid-rich (LM), P/S 0.19; palmitic acid-rich (POL), P/S 0.31; and stearic acid-rich (STE), P/S
0.22. Blood was sampled at fasted baseline and 2, 4, 5, 6, and 8 hours. Plasma lipids (triacylglycerol [TAG]) and
lipoproteins (TC, LDL-C, high density lipoprotein-cholesterol [HDL-C]) were evaluated.
Results: Varying SFA in the test meal significantly impacted postprandial TAG response (p , 0.05). Plasma
TAG peaked at 5 hours for STE, 4 hours for POL, and 2 hours for LM test meals. Area-under-the-curve (AUC)
for plasma TAG was increased significantly after STE treatment (STE . LM by 32.2%, p¼ 0.003; STE . POL
by 27.9%, p¼ 0.023) but was not significantly different between POL and LM (POL . LM by 6.0%, p . 0.05).
At 2 hours, plasma HDL-C increased significantly after the LM and POL test meals compared with STE (p ,
0.05). In comparison to the STE test meal, HDL-C AUC was elevated 14.0% (p¼ 0.005) and 7.6% (p¼ 0.023)
by the LM and POL test meals, respectively. The TC response was also increased significantly by LM compared
with both POL and STE test meals (p , 0.05).
Conclusions: Chain length of saturates clearly mediated postmeal plasma TAG and HDL-C changes.
INTRODUCTION
A lower fat consumption with reduction in saturated fatty
acid (SFA) content of the total diet has been an important
strategy for the past 5 decades of cardiovascular disease (CVD)
risk management associated with hypercholesterolemia [1–3].
Dietary fatty acid type is well established to affect total
cholesterol (TC) with parallel changes in low density
lipoprotein-cholesterol (LDL-C) [4,5] and is in agreement
with predictive coefficients [4,6,7]. A meta-analysis of the
National Cholesterol Education Program (NCEP) Step II diet
studies incorporating ,7% SFA calories have reported an
achievable 16% decrease in LDL-C level [8].
A counterpoint to SFA reduction is an effect causing a
reduction in high density lipoprotein-cholesterol (HDL-C)
concentration. Three randomized controlled trials in humans
have shown that diets providing 6%–7% SFA calories
produced a 9%–11% reduction in LDL-C accompanied by a
7%–11% reduction in HDL-C [9–11]. Of these, a 9% increase
in plasma triacylglycerol (TAG) was observed in one study
[10]. Consuming ;4% SFA calories reported by one
randomized controlled trial achieved an 8.6% reduction in
LDL-C and a 10% reduction in HDL-C [12]. The Delta,
OmniHeart Randomized Trial, Dietary Alternatives, and beFIT
studies have demonstrated that limiting SFA calories by
Address reprint requests to: Kalyana Sundram, PhD, Malaysian Palm Oil Council, Kelana Jaya, Selangor, MALAYSIA. E-mail: [email protected]
Supported by a grant from the Ministry of Science, Technology and Innovations, Kuala Lumpur, Malaysia (E-Science Grant No. 06-01-02-SF0313).
None of the authors have a conflict of interest to declare.
Abbreviations: C12:0þC14:0 ¼ lauric þ myristic acids, C16:0 ¼ palmitic acid, C18:0 ¼ stearic acid, FAC ¼ fatty acid composition, HDL-C ¼ high density lipoprotein-
cholesterol, LDL-C¼ low density lipoprotein-cholesterol, LM¼ lauricþmyristic acid-rich diet, MUFA¼monounsaturated fatty acid, POL¼palmitic acid-rich diet, PUFA
¼ polyunsaturated fatty acid, SFA¼ saturated fatty acid, STE¼ stearic acid-rich diet, TAG¼ triacylglycerol, TC¼ total cholesterol, TRL¼ triglyceride-rich lipoproteins.
Journal of the American College of Nutrition, Vol. 30, No. 6, 511–521 (2011)
Published by the American College of Nutrition
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exchanging with carbohydrates increased plasma TAG and
decreased HDL-C [11,13–15].
Atherogenic potential of SFA is not uniform as at a high fat
energy intake, myristic acid (C14:0) is the most hypercholes-
terolemic, with a suggested potency 3–6 times greater than
lauric (C12:0) or palmitic (C16:0) acids, whereas stearic acid
(C18:0) has been suggested to be neutral [16,17]. The
TC:HDL-C ratio has been shown in a meta-analysis by
Mensink et al. [7] to decrease with increasing saturation from
C12:0- to C18:0-rich diets. A recent systematic review
indicated that when C18:0 was substituted for other SFA,
LDL-C decreased but remained unchanged when substituted
for carbohydrate [18]. A proposed recommendation of the 2010
DGAC [19] was to support C18:0-rich foods, such as cocoa
butter (dark chocolate) or shea nut oil, as ‘‘not problematic’’
compared with other types of SFA-rich vegetable oils.
However, the 2010 DGAC report [19] also concluded that
the impact of substituting C18:0 for other energy sources was
variable regarding LDL-C, and the potential impact of changes
in C18:0 intake on CVD risk remained unclear.
Since 2000 the NCEP Adult Treatment Panel III guidelines
through the Therapeutic Lifestyle Changes have promoted
global risk management for CVD to target hypertriglyceride-
mia, thrombogenecity, and inflammation while achieving low
TC and LDL-C [20,21]. Hypertriglyceridemia and low HDL-C
are now identified as new risks for coronary artery disease in
association with ‘‘low metabolic capacity.’’ The dyslipidemic
environment is prone to prolonged postprandial lipemia, which
is associated with unfavorable hemostatic dynamics. Impaired
reverse cholesterol transport is now identified as a source of
inflammatory and thrombogenic triacylglycerol-rich lipopro-
teins (TRL) rising from absorption of dietary lipids [22,23].
Studies that evaluate the contributory role of fat to postmeal
hypertriglyceridemia are limited [24,25]. One study by Kralova
et al. [25] questioned whether reduced HDL-C on a high
polyunsaturated fatty acids (PUFA)/low SFA diet affected
reverse cholesterol transport negatively but did not find any
difference in cholesterol efflux. Given this new era of global
risk management in CVD, we undertook to compare the effects
of different SFAs on postprandial lipemia in normocholester-
olemic subjects.
MATERIALS AND METHODS
Subjects
A total of 20 normolipemic healthy subjects, 10 men and 10
women aged between 22 to 38 years without a history of
atherosclerotic disease or hypertension were recruited into the
study. Female subjects were nonpregnant and nonlactating, and
none of the subjects were on any prescribed medication.
Subjects were nonsmokers, consumed no alcohol, and did not
take any nutritional supplements or participate in weight-loss
programs immediately prior to or during the study. Addition-
ally, female subjects ceased use of oral contraceptives. Subjects
were thoroughly briefed on the study protocol and gave their
written informed consent for participation in the study. They
had the freedom to drop out from the study at any time.
Subjects participated in an initial screening and their baseline
characteristics were as follows: age, 30.1 6 8.03 years; body
mass index (BMI), 22.5 6 4.40 kg/m2; TC, 4.97 6 0.58 mmol/
L; TAG, 0.94 6 0.32 mmol/L; LDL-C, 2.96 6 0.54 mmol/L;
and HDL-C, 1.58 6 0.31 mmol/L.
Study Design
The study was designed to evaluate postprandially the effect
of varying chain length saturation of dietary fats on lipids and
lipoproteins. Blending coconut oil with corn oil provided a
lauric þ myristic-rich (LM) fat with a polyunsaturated to
saturated fatty acid ratio (P/S) of 0.19, whereas a stearate-rich
fat (STE, P/S ¼ 0.22) was obtained by blending cocoa butter
with corn oil. In contrast, palm olein on its own provided a
predominantly palmitic acid-rich fat (POL, P/S ¼ 0.31).
Formulated test fats were rotated in a randomized crossover
design, with all subjects consuming experimental diets
containing a test fat for 7 days prior to a postprandial challenge
on the morning of the eighth day. A 7-day washout separated
test fat rotations. In each test-fat rotation, subjects were
assigned to 2 groups of 10 each to optimize the proper and
correct handling of blood specimens within the time constraints
imposed by the study design. Female subjects were assigned
between menses to the experimental groups. Subjects were
instructed to eat according to their usual individual food intake
patterns and were blinded to the test fats used for each rotation.
Body weight measurements were recorded before each
postprandial challenge to ensure weight fluctuations were
minimized between the test rotations. This study protocol was
approved by the institutional ethics committee.
Test Meals
A standard 7-day menu plan was adopted for all test fat
rotations. The test meals were eucaloric and differed only in the
composition of the incorporated test fats. This was confirmed
by actual fatty acid composition (FAC) of the test fats and
duplicated portions of test meals as consumed by the volunteers
(Table 1). All meals were eucaloric in their macronutrient
composition but differed in their FAC. The major SFA in the
test meals reflected the test fats, as evidenced by the content
(%) of C16:0 in the POL diet, C12:0 and C14:0 in the LM diet,
and C18:0 in the STE diet. The percentage linoleic acid (C18:2)
in terms of energy content across all test fats (;11% en) and
test meals (;3% en) was adjusted to be similar and to yield
overall low P/S ratios (0.19–0.31). The daily menu during the
7-day run-in period provided approximately 50 g of the test fat
in the diet, equivalent to ;26% en. Thus total daily fat content
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Dietary Saturate Type Affects Postprandial Lipemia
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of test meals provided during each of these periods was
maintained at 31% en with the remainder (;5% en) coming
from dietary sources of invisible fats.
The menu used typical Malaysian recipes and was
constructed according to the following meal plan: (1) for
breakfast, a cereal dish and a snack item cooked with the test
fat was served with either coffee or tea, (2) lunch included fish
or chicken and two vegetables cooked with the test fat and
accompanied by rice and fruits, and (3) for high tea, a snack
item with the test fat incorporated was served with either tea or
coffee. All meals were prepared by a trained caterer and
standardized to recipes and portion sizes. Procedures for
incorporating the test fats were supervised during meal
preparations by a dietitian. To maximize compliance, subjects
were provided with the test fats for preparation of dinner and
for weekend meals at home. On the eighth morning, subjects
were challenged with the postprandial test meals.
Postprandial Challenge
Subjects were advised to refrain from strenuous physical
activity for 24 hours preceding each postprandial event. They
reported to the laboratory at 0800 hours on the day assigned for
the postprandial fat challenge after an overnight minimum fast
of 10 hours. A 12-ml fasted venous blood sample was obtained
from each subject. Subjects then consumed the postprandial
meal challenge containing the test fat within 15 minutes of
drawing the fasted blood sample. The potprandial meal
challenge consisted of fried rice and a breaded snack using
the test fat specific to the test rotation and as described in Table
1. This meal consisted of 275 g of fried rice with 2 portions of
breaded snack that provided approximately 960 kcal, 50 g fat
(47% en), 98 g carbohydrate (41% en), and 29 g protein (12%
en). Plain tea or coffee was allowed with the test meal.
Chemical analyses of randomized samples of postprandial test
meal challenges confirmed a mean fat content of 47.38 6 11.63
g. Only the consumption of mineral water was allowed ad
libitum for the ensuing 8 hours of the postprandial period. On
completion of the postprandial sessions, subjects were provided
with a cooked meal. Subjects remained in a rested state during
the 8 hours of the postprandial challenge.
Twelve-ml blood samples were drawn by venous puncture
from fasting subjects at 0 hours (i.e., before the meal challenge)
and subsequently at 2, 4, 5, 6, and 8 hours after the
consumption of the test-fat challenges. The same sequence of
blood sampling for all timed events was followed during each
postprandial challenge. Blood sampling at each time point was
completed for all subjects within 15 minutes of beginning the
session.
Blood Sampling and Biochemical Determination
Blood was collected into Vacutainert tubes (Becton Dick-
inson Vacutainer, Franklin Lakes, NJ) containing EDTA
(0.117 ml of 15% EDTA) and immediately centrifuged at
3000g for 20 minutes at 48C (Sigma 3K12, B. Braun,
Tuttlingen, Germany) to separate the plasma from red blood
cells. Fresh plasma was reserved for ultracentrifugation,
whereas the remaining plasma was aliquoted and snap-frozen
in liquid nitrogen and stored at�808C for subsequent analyses.
Isolation of TRLs
Ultracentrifugation of fresh EDTA plasma to extract TRL-
rich chylomicrons was carried out in sealed Beckman Quick-
Sealt polyallomer tubes (Beckman Instruments Inc., Palo Alto,
CA) as per procedures of the Lipid Research Clinics Programs
of the National Institutes of Health/National Heart and Lung
Institute in the United States [26]. Each Quick-Sealt tube was
set upright in a holder and a long-tipped Pasteur pipette was
introduced through the narrow neck of the tube. The Pasteur
pipette served as the conduit for addition of 0.9% sodium
chloride (NaCl) (specific density, d ¼ 1.006) and plasma.
About 3.5 ml of NaCl was delivered into the Quick-Sealt tube
without introducing air bubbles. Then, 3 ml of EDTA plasma
was layered under NaCl, without introducing air bubbles. The
Pasteur pipette was carefully withdrawn without disturbing the
plasma and NaCl phases. The final volume in the Quick-Sealt
tube was topped with NaCl using a fine-bore 1.0-ml syringe
before sealing the neck of the tube with a tube sealer (Beckman
Instruments).
Sealed and labeled Quick-Sealt tubes were ultracentrifuged
for 18 hours at 47,000g at 128C with a type 50.3 Ti fixed angle
Table 1. Fatty Acid Composition of the Test Fats and Test
Meals*
Fatty Acids
Test Fats
(% Total Fat)
Test Meals
(% Total en)�
POL LM STE POL LM STE
Total SFA 44.05 74.74 59.13 10.99 17.03 13.48
C8:0 nd 4.71 nd nd 0.89 0.02
C10:0 nd 3.96 nd nd 0.77 0.03
C12:0 0.23 40.83 nd 0.36 7.43 0.37
C14:0 0.9 14.15 nd 0.40 2.97 0.25
C16:0 38.82 8.91 25.76 8.96 3.85 6.57
C18:0 4.1 2.18 33.37 1.27 1.12 6.23
MUFA 44.45 20.93 34.47 11.56 5.44 8.96
C18:1 43.58 20.09 33.62 11.33 5.22 8.74
PUFA 11.58 11.67 11.58 3.35 3.24 2.92
C18:2 11.23 11.44 10.61 3.26 3.11 2.77
C18:3 0.35 0.23 0.97 0.09 0.13 0.15
P/S ratio 0.26 0.16 0.20 0.31 0.19 0.22
* POL ¼ palm olein only, LM ¼ lauric þ myristic acid-rich oil obtained from
blending coconut and corn-oils, STE¼ stearic-acid rich oil obtained by blending
cocoa butter with corn oil, SFA¼ saturated fatty acid, MUFA¼monounsaturated
fatty acid, PUFA ¼ polyunsaturated fatty acid, nd ¼ not detectable, P/S ratio ¼polyunsaturated / saturated fatty acid ratio.� % total en ¼ percentage energy of total fat in the meal.
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION 513
Dietary Saturate Type Affects Postprandial Lipemia
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rotor (Beckman Instruments). At the end of ultracentrifugation,
Quick-Sealt tubes were sliced at the point of sealing, and
aliquots were removed in sequence. First, a precise 2.0-ml
aliquot from the top fraction yielding TRL (d , 1.006 g/ml)
was transferred by aspiration with a Pasteur pipette into a clean
test tube for storage at �408C. This fraction was reserved for
further analysis. The remaining bottom fraction was recovered
separately and made up to a final volume of 3.0 ml with NaCl
solution (d . 1.006 g/ml). This fraction was subsequently used
to determine HDL-C concentration (d¼ 1.063 g/ml) as well as
to characterize plasma cholesteryl ester (CE) FAC.
Lipids and Lipoproteins
The TC in plasma and cholesterol content of TRL and
bottom fractions of ultracentrifuged plasma were determined by
enzymatic procedures [27]. Plasma TAG was also similarly
determined [28]. A precise 35-ll volume of dextran sulfate-
Mg2þ precipitating agent was added to 350 ll of the bottom
fraction, the mixture vortexed and the reaction timed for 10
minutes to precipitate LDL [29,30]. The clear supernatant,
obtained through centrifugation for 10 minutes at 7000g
(Speedfuge HSC10K, Savant Instruments Inc., Farmingdale,
NY), was used to determine HDL-C content. All assays were
performed using a Ciba-Corning 550 Express Autoanalyzer
(Ciba-Corning Diagnostics Corp., Oberlin, OH). Reagents,
calibrators, and controls were supplied by Bayer Corp.
(Tarrytown, NY), and the HDL-C precipitant was supplied
by Chiron Diagnostics Corp. (Emeryville, CA). Plasma LDL-C
was calculated by the differences between cholesterol content
of the bottom fraction of ultracentrifuged plasma and HDL-C
[26,31].
Fatty Acid Composition
Two milliliters of the upper fraction of ultracentrifuged
plasma containing TRL were used for lipids extraction by the
Folch method [32]. The CE were similarly extracted from the
bottom fraction of ultracentrifuged plasma samples [32].
Extracted lipids were then subjected to thin-layer chromato-
graphic separation with a mixed solvent phase of hexane,
diethyl ether, and acetic acid (80:20:2). Lipids from double-
portioned meals were obtained by Soxhlet extraction [33].
Extracted lipids from TRL, CE, and test meals were converted
into fatty acid methyl esters, dried under nitrogen, and
reconstituted with hexane before injection into the gas
chromatographer (Perkin-Elmer Autosystem, Perkin-Elmer,
Norwalk, CT). The FAC of TRL, CE, and test meals were
expressed as percentage composition (by weight), calculated by
reference to authentic standards [33]. The FAC of the meals
consumed by the subjects served to check whether the test
meals achieved targeted FAC, whereas the FAC of subjects’
plasma served to check compliance to the study protocol.
Statistical Analyses
The crossover design enabled every subject to serve as his
or her own control; all 20 subjects completed the 3 test-meal
rotations. The Statistical Package for Social Sciences, SPSSt
for WindowsTM application (Version 15.0, SPSS Inc., Chicago,
IL) was used for the required statistical analyses. Differences
between outcomes from the various postprandial time intervals
and baseline values (0 hour) were interpreted as true measures
of change resulting from dietary treatment. Multivariate
analyses for repeated measures (MANOVA), using the general
linear model, was performed for all time 3 test meal values for
each measurement parameter. Univariate analysis was used to
compare the area-under-the-curve (AUC) derived for the 8-
hour duration of the postprandial period calculated by the
trapezoidal rule [34]. The Levene test was used to examine
equality of variances across treatment groups. Bonferroni
adjustment for multiple paired comparisons was used to test
mean differences between groups. Significance was set at p ,
0.05 for all evaluated measures.
RESULTS
Subject Demographics at Baseline
All 20 subjects successfully completed the 3 test rotations.
A nonsignificant increase in body weight of 0.62 6 0.78 kg
from baseline to study completion was evident.
Lipemic Response and Test Fat Clearance
Changes in plasma TAG (mean 6 SD) occurring over timed
intervals in response to 3 postprandial test fat challenges are
presented in Fig. 1a,b. Dietary saturates caused highly
significant (p ¼ 0.002) time 3 meal treatment changes to
plasma TAG concentrations during the 8-hour postprandial
period (Fig. 1a). The magnitude and extent of plasma TAG
response was greatest after feeding the C18:0-rich STE fat
challenge and attained significance in comparison to the C16:0-
rich POL (p ¼ 0.023) and C12:0þC14:0-rich LM (p ¼ 0.003)
meals in pairwise comparisons of the estimated marginal
means. AUC confirmed that the variable effect of the dietary
saturates was significantly different (p¼0.016) and greatest for
the STE treatment (STE . LM by 32.2%, STE . POL by
27.9%), versus the comparison between the POL and LM test
meals (POL . LM by 6.0%) (Fig. 1b). The effect was
significant from 2 hours onward (p , 0.05), and differences in
lipemic clearance was evident, with plasma TAG peaking at 5
hours for the C18:0 meal, 4 hours for the C16:0 meal, and 2
hours for C12:0þC14:0 meal, indicating fat clearance was in
the order of C12:0þC14:0 . C16:0 . C18:0. It was further
observed that lipemic response generated by STE meal did not
resume postabsorptive levels by 8 hours, unlike responses after
the POL and LM treatments.
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Plasma TC, LDL-C, and HDL-C
Changes in plasma lipoprotein concentrations occurring
over time in response to the 3 postprandial test fat challenges
(time 3 diet interactions) are presented in Figs. 2a,b; 3a,b; and
4a,b. Postprandial TC responses were not significantly affected
by the type of saturates tested (Fig. 2a) except for a time effect
from 5 to 8 hours (p¼ 0.026) for all meals, with a significantly
higher increase after the LM challenge compared with the POL
and STE treatments (p ¼ 0.033). TC response after POL and
STE treatments was not significantly different. Overall, AUC
for TC did not result in any significance between different
saturates (Fig. 2b).
Initial HDL-C concentrations decreased at baseline for all
meals, but after 2 hours an upward trend was observed for the
LM and POL test meals but not for the STE meal (Fig. 3a).
Treatment effect became significant (p¼0.003) after correcting
for baseline values as well as for pairwise comparisons of
estimated marginal means between the STE and POL
treatments (p ¼ 0.023) and for the STE and LM treatments
(p¼ 0.005). Differences between the LM and POL treatments
were not significant. AUC was not significantly different from
baseline (Fig. 3b). Percentage increase in AUC plasma HDL-C
was 14.0% greater for the LM compared with the STE
treatments (p ¼ 0.005) and 7.6% between the POL and STE
treatments (p ¼ 0.023).
LDL-C concentrations for all saturates were elevated toward
the end of the measured postprandial event, but this elevation
was not significantly different between treatments (Fig. 4a).
AUC for LDL-C response also did not achieve significance
between the dietary saturates tested (Fig. 4b).
FAC Patterns of TRL and CE
The effect of time was not significant after correction for the
baseline values for individual fatty acids in both TRL and CE.
Fig. 5a–d indicates the distribution of individual fatty acids
(mean 6 SE) in TRL, expressed as a percentage of the FAC. A
Fig. 1. (a) Plasma TAG (mean 6 SEM, n¼ 20) concentrations over 8 hours in response to test meals containing POL, LM, or STE oil type. Repeated
measures MANOVA analyzed for time 3 test meal interactions was significant (p¼ 0.002). The lipemic trend generated by the C18:0-rich STE meal
was greater than that of the C16:0-rich POL (p ¼ 0.023) or LM (p ¼ 0.003) test meals. (b) Univariate analyses on AUC for plasma TAG was
significantly higher for the STE test meal (p ¼ 0.016) compared with the LM (.32.2%) and POL (.27.9%) test meals, whereas the difference
between the POL and LM test meals (6.0%) was not significant. POL ¼ palm olein only (¤), LM ¼ lauric þ myristic acid-rich oil obtained from
blending coconut and corn oils (&), STE¼ stearic acid-rich oil obtained by blending cocoa butter with corn oil (m).
Fig. 2. (a) Plasma TC response (mean 6 SEM, n¼ 20) over 8 hours following a standardized fat load with the POL, LM, or STE test meals. Repeated
measures MANOVA analysis for time 3 test meal interactions was not significant (p , 0.05). An effect of time was significant from 5 to 8 hours (p¼0.026) with significantly greater plasma TC response generated by the LM compared with the POL and STE test meals (p¼ 0.033). (b) Univariate
analyses for AUC of plasma TC was not significantly different. POL ¼ palm olein only (¤), LM ¼ lauric þ myristic acid-rich oil obtained from
blending coconut and corn oils (&), STE¼ stearic acid-rich oil obtained by blending cocoa butter with corn oil (m).
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significant effect of dietary treatment (p , 0.05) was evident
for lauric þ myristic (C12:0þC14:0), palmitic (C16:0), stearic
(C18:0), and linoleic (C18:2) acids in the composition of TRL.
C12:0þC14:0 in TRL was significantly higher after LM
treatment (p , 0.001) compared with the POL and STE
treatments, an effect attributed to their dietary availability (LM
¼ 40.0%; POL ¼ 2.9%; STE¼ 2.4%). Incorporation of C16:0
into TRL was greatest after the POL test meal compared with
the LM and STE meals (p , 0.001) as expected due to its
greater dietary availability (POL¼34.5%; LM¼14.8%; STE¼25.3%), but surprisingly, despite the lowest content of C16:0 in
the LM meal, incorporation into TRL was not significantly
different between the STE and LM meals. It was noted that
percentage C16:1n7 was not significantly different (p . 0.05)
between diets (data not shown). Percentage C18:0 in TRL was
significantly (p , 0.001) related to dietary availability (POL¼4.9%; LM ¼ 4.3%; STE ¼ 23.9%) with the greatest
incorporation after the STE treatment and minimal after the
POL and LM meals. C18:1 in TRL (p , 0.001) reflected
dietary source (POL ¼ 43.6%; LM ¼ 20.1%; STE ¼ 33.6%),
and incorporation appeared to be dose-dependent with POL .
LM (p , 0.001), POL . STE (p , 0.001), and STE . LM (p
¼ 0.024). Presence of C18:2 in TRL was significantly higher
after the LM treatment compared with the POL (p , 0.001)
and STE (p , 0.001) treatments, and this was independent of
the C18:2 content of the meals (POL ¼ 12.5%; LM ¼ 12.0%;
STE ¼ 10.7%). Though data are not shown here, percentage
C18:1 was significantly affected by test meal treatment (p ,
0.05) in the order of POL . STE . LM.
Individual fatty acid concentrations in CE as percentage
FAC, in response to the various SFA test meals are presented in
Fig. 6a–d. Significant differences in the CE fatty acids after
correction for baseline values were evident for C12:0þC14:0 (p
, 0.001), C16:0 (p¼ 0.001), C18:0 (p , 0.001), and C18:1 (p
, 0.001). The appearance of these fatty acids in CE reflected
meal source but were independent of test meal 3 time
interactions.
Fig. 3. (a) Plasma HDL-C (mean 6 SEM, n ¼ 20) concentrations over 8 hours in response to test meals containing POL, LM, or STE test fats.
Repeated measures MANOVA analyzed for time 3 test meal interactions was significant (p¼ 0.003) and comparisons between meals was significant
between the STE and POL (p¼ 0.023) meals and the STE and LM (p¼ 0.005) meals but not between the LM and POL meals. (b) AUC for plasma
HDL-C (means 6 SEM, n¼ 20) as analyzed by univariate analysis was not significantly different from baseline except at 2 hours (p¼ 0.055), for
which the STE meal was 14.0% greater compared with the LM (p¼ 0.005) and 7.6% greater compared with the POL (p¼ 0.023) meals. POL¼ palm
olein only (¤), LM¼ lauricþmyristic acid-rich oil obtained from blending coconut and corn oils (&), STE¼ stearic acid-rich oil obtained by blending
cocoa butter with corn oil (m).
Fig. 4. (a) Plasma LDL-C (mean 6 SEM, n ¼ 20) concentrations over 8 hours in response to test meals containing POL, LM, or STE test fats.
Repeated measures MANOVA analyzed for time 3 test meal interactions were not significant (p . 0.05). (b) No significant difference for plasma
LDL-C AUC (mean 6 SEM, n ¼ 20) was noted between test meals (p . 0.05). POL ¼ palm olein only (¤), LM ¼ lauric þ myristic acid-rich oil
obtained from blending coconut and corn oils (&), STE¼ stearic acid-rich oil obtained by blending cocoa butter with corn oil (m).
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DISCUSSION
A potential novelty of this study is that plasma fatty acids of
TRL and CE fractions isolated from chylomicrons and plasma,
respectively, have been reported for a postprandial study. Their
fatty acid patterns clearly are traced back to the FAC of the
dietary fats used in the postprandial challenges. These,
therefore, may assist in enhancing our understanding of the
dynamics of different dietary fatty acids during fat metabolism.
Differences arising from postprandial response to the various
fats tested in this study are directly attributed to the chain
length of dietary saturates tested. The FAC of test fats and their
incorporation into the respective test meals reflected the highest
contents of C16:0 (34.5%) in POL, C12:0þC14:0 (40.0%) in
LM, and C18:0 (24.0%) in STE meals, respectively. This was
anticipated because palm olein as the POL test fat is a rich
source of C16:0 and coconut oil provided the higher
C12:0þC14:0 in the LM test fat, whereas the higher C18:0
content of the STE test fat was provided by cocoa butter. Corn
oil was added to the LM and STE test meals to equalize the
PUFA content among all meals. Only the MUFA content of the
test meals differed.
The postprandial response of plasma TAG to dietary
saturates was affected by the predominant SFA in the test
meals and indicated a trend based on the carbon chain length of
the fatty acids tested. Magnitude of lipemic response was
greatly enhanced by the C18:0-rich STE meal and in the
following order, C18:0 . C16:0 . C12:0þC14:0. Lipemia
associated with the C18:0-rich STE meal was enhanced and
prolonged for the postprandial duration of 8 hours compared
with the C12:0þC14:0-rich LM meal and the C16:0-rich POL
meal. Preferential fat clearance has been noted between fat
classes such as PUFAs, MUFAs, and SFAs but not within a
SFA class. Both Zampelas et al. [35] and Demacker et al. [36]
attributed a slower return to the postabsorptive state to long-
chain SFAs compared with PUFAs. Thomsen et al. [37] found
TAG in the chylomicron-rich fraction of plasma to rise 2.5-fold
to fivefold on a butter-rich meal compared with a corn-oil-rich
meal. In contrast Mekki et al. [38] found a lower lipemia and
chylomicron accumulation on a butter-rich meal compared with
Fig. 5. Fatty acid composition (FAC) of triacylglycerol (TAG) in
triacylglycerol-rich lipoproteins (TRL) (mean % 6 SEM, n ¼ 20) in
response to test meals containing POL, LM, or STE test fats. Statistical
analyses were corrected for baseline values and significance reported at
p , 0.05 for time 3 meal interactions. (a) Percentage C12:0þC14:0
increased significantly after LM meal compared with the POL and STE
meals (p , 0.05), whereas comparisons between POL and STE were
not significantly different (p . 0.05). (b) Percentage C16:0 increased
significantly after the POL meal compared with the LM and STE meals
(Fig. 5. Continued.)
(p , 0.05), whereas comparisons between LM and STE were not
significantly different (p . 0.05). (c) Percentage C18:0 increased
significantly after the STE meal compared with the POL and LM meals
(p , 0.05), whereas comparisons between POL and LM were not
significantly different (p . 0.05). (d) Percentage C18:1 increased
significantly after the POL meal compared with the STE and LM meals
(p , 0.05), whereas comparisons between STE and LM were not
significantly different (p . 0.05). POL ¼ palm olein only (¤), LM ¼lauricþmyristic acid-rich oil obtained from blending coconut and corn
oils (&), STE¼ stearic acid-rich oil obtained by blending cocoa butter
with corn oil (m).
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olive-oil-rich and sunflower-oil-rich meals. Asakura et al. [39]
also found a lower lipemia associated with medium-chain SFA-
rich compared with an n-6 PUFA-rich fat challenges.
Plasma TAG clearance appeared to be affected by chain
length of the dietary saturates tested. Peaking time was earlier
with the LM meal at 2 hours, slowest with the STE meal at 5
hours, and 4 hours with the POL meal. The particle size of
TRL-rich chylomicrons is hypothesized to affect postprandial
fat clearance. Unsaturated fatty acids reportedly increase
particle size compared with SFAs [40,41]. Circulating
chylomicrons were smaller after a butter-rich meal compared
with PUFA- and MUFA-rich meals [38]. It is, therefore,
possible that the carbon-chain length of the different saturates
tested in this study affected particle size and number of
chylomicrons during lipemia. This may perhaps explain the
association of the slowest clearance after the C18:0-rich meal
and the rapid clearance after the C12:0þC14:0-rich LM meal.
Preferential hydrolysis by lipoprotein lipase may also be linked
to the differences in fat clearance seen for the different saturates
tested [42,43].
A prolonged and higher lipemia is conducive to a
prothrombotic state due to the exaggerated and prolonged
presence of TAG-rich TRL in the circulation [23,24].
Postprandial lipemia has been shown to increase levels of
factor VIIa (FVIIa) and plasminogen activator inhibitor 1
[44,45]. Activation of factor VII (FVII) has been observed in
healthy adults and in those with congenital deficiency of either
factors XI or XII after a high-fat meal [46]. However the
contributory effects of fat composition to thrombogenecity is
unclear at present, given that mixed findings have been
reported. Feeding olive oil lowered FVIIa response compared
with either rapeseed or sunflower oils, but associated lipemia
was significantly higher for olive oil. Sanders et al. [47]
compared randomized and unrandomized cocoa butter in
healthy subjects and found that unrandomized cocoa butter,
rich with C18:1 in the sn-2 position, was absorbed more rapidly
than randomized cocoa butter, which predominated in C18:0 in
the sn-2 position. This, they concluded, led to increased
activation of FVII associated with the unrandomized cocoa
butter. A randomized control trial (n ¼ 96) found FVIIa
response to a fat-rich meal was independent of its fatty acid
Fig. 6. Fatty acid composition (FAC) of plasma cholesteryl esters
(CE) (mean % 6 SEM, n ¼ 20) in response to test meals containing
POL, LM, or STE test fats. Statistical analyses were corrected for
baseline values and significance reported at p , 0.05 for time 3 test
meal interactions. (a) Percentage C12:0þC14:0 increased significantly
after the LM meal compared with the POL and STE meals (p , 0.05),
whereas comparisons between POL and STE were not significantly
different (p . 0.05). (b) Percentage C16:0 increased significantly after
the POL meal compared with the LM and STE meals (p , 0.05),
whereas comparisons between LM and STE were not significantly
(Fig. 6. Continued.)
different (p . 0.05). (c) Percentage C18:0 increased significantly after
the STE meal compared with the POL and LM meals (p , 0.05),
whereas comparisons between POL and LM were not significantly
different (p . 0.05). (d) Percentage C18:1 was significantly greater
after the POL and STE meals compared with the LM meal (p , 0.05),
whereas comparisons between POL and STE were not significantly
different (p . 0.05). POL ¼ palm olein only (¤), LM ¼ lauric þmyristic acid-rich oil obtained from blending coconut and corn oils (&),
STE¼ stearic acid-rich oil obtained by blending cocoa butter with corn
oil (m).
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composition, and not influenced by the different degree of
lipemia of the C18:2/18:3 rich meal compared with C16:0 and
C18:0 [48].
HDL-C response in this study was also influenced by chain-
length of the dietary saturates, which increased with decreasing
SFA chain length in the order of C12:0þC14:0 . C16:0 .
C18:0. The postprandial HDL-C response saw an increase after
the LM and POL diets but remained depressed for the STE
meal. The significant change in HDL-C concentration that was
observed for the LM and POL meals occurred 2 hours after the
postprandial meal challenge. The postprandial trend observed
for HDL-C may be linked to the differences in fat clearance
that occurred as a result of the different saturates. Only
Thomsen et al. [37] have reported a difference in HDL-C
response when comparing olive oil and butter. In their study a
higher HDL-C response associated with the olive oil meal was
in tandem with a faster fat clearance. It remains to be explored
whether differences seen in postprandial HDL-C response
attributed to different saturates are linked to fat clearance and
whether this is mediated through reverse cholesterol transport.
CONCLUSION
Individual dietary saturates, as this study demonstrated,
variably affected postprandial plasma TAG and lipoproteins.
The nature of dietary saturates clearly influenced fat digestion
and absorption in the subjects. The magnitude of lipemic
response was greatest for a stearic acid-rich (C18:0) meal and
least for a lauricþmyristic-rich (C12:0þC14:0) meal. Similarly
the HDL-C response was affected by the chain length of
saturates, albeit inversely. HDL-C concentrations were highest
with the C12:0þC14:0-rich meal and decreased with increasing
carbon-chain length of the fatty acid tested. In contrast, the
responses elicited by the palmitic acid-rich (C16:0) meal, on
lipemia and HDL-C, were moderate compared with LM and
STE.
ACKNOWLEDGMENTS
The contribution of each author is as follows: T.K., an
accredited practicing dietitian, was responsible for data
acquisition and drafting of this manuscript; C.H.T. was a
graduate student participating in the implementation of the
study; K.C. was responsible for statistical analyses and
interpretation of data; K.S. made substantial contributions to
conception and design of the study and finalization of the
manuscript. None of the authors have a conflict of interest to
declare. This research protocol was approved by the Ethical
Approval Committee of the National University of Malaysia
with the registration number FF-165-2007.
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