© 1998 American Heart Association, Inc.
Original Contributions |
Similar Effects of Diets Rich in Stearic Acid or trans-Fatty Acids on Platelet Function and Endothelial Prostacyclin Production in Humans
From the Department of Applied Chemistry and Microbiology (Nutrition), University of Helsinki, Helsinki, Finland (A.M.T., M.M.); the Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Munich, Germany (J.W., R.L.); and the Department of Nutrition, National Public Health Institute, Helsinki, Finland (A.A.).
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Abstract |
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Abstract—The effects of stearic acid (C18:0) and trans-fatty acids (trans-FAs) on measures of platelet function and prostacyclin (PGI2) production are poorly understood in humans. In this controlled dietary study, platelet function and endothelial PGI2 production were studied in healthy humans after they consumed diets rich in C18:0 or trans-FAs. For 5 weeks, 80 subjects consumed a baseline diet high in saturated FAs and were then switched to a diet containing 9.3% of energy as stearic acid or a diet containing 8.7 energy% as trans-FAs from hydrogenated vegetable oils for another 5 weeks. All diets contained 32.2 to 33.9 energy% fat, 14.6 to 15.8 energy% saturated plus trans-FAs, 12.2 to 12.5 energy% cis-monounsaturated, and 2.9 to 3.5 energy% polyunsaturated FAs. No significant differences between the C18:0 and trans-FA diets were found in the urinary excretion of 2,3-dinor-thromboxane B2 or 2,3-dinor-6-keto-prostaglandin F1
. In
vitro production of thromboxane B2 by
platelets as well as urinary excretion of
ß-thromboglobulin were also similar after both
diets. Collagen-induced in vitro aggregation was significantly enhanced
after the C18:0 diet compared with the trans-FA
diet (P=.02), whereas no differences between the diets
were found with ADP. The results indicate similar effects of C18:0 and
trans-FA diets on platelet activation and
endothelial PGI2 production.
Key Words: stearic acid • trans-fatty acids • platelet activation • 2,3-dinor-TXB2 • 2,3-dinor-6-keto-PGF1
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Introduction |
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Strong evidence from human dietary intervention studies suggests that trans-FAs have unfavorable effects on risk factors for coronary heart disease. Studies that have mainly focused on lipoprotein metabolism have mostly shown increased LDL1 2 3 and decreased HDL1 2 concentrations after consumption of diets with varying amounts of monounsaturated trans-FAs. Increased lipoprotein(a) concentrations have also been reported,3 4 although this observation has not been consistent.5 6 Still, data on the thrombogenic properties of these FAs are mostly based on animal studies or in vitro studies with isolated cells. In rats, trans-FAs have inhibited thromboxane production7 and either inhibited8 or had no effect9 on platelet aggregation.
It is apparent that stearic acid has a different cholesterolemic effect than other long-chain saturated FAs. Regarding lipoprotein metabolism, stearic acid has been considered neutral with respect to total cholesterol and LDL cholesterol, although HDL cholesterol has decreased in some studies.10 11 12 Whether stearic acid can also be considered neutral with respect to its thrombotic effects is unclear. Evidence from human epidemiological and animal studies suggests that stearic acid enhances platelet aggregation in vitro, indicating its effects on platelet activity, an important aspect of thrombosis and hemostasis.13 14 15 In vivo indices of platelet activation have been measured in only one human study, in which thromboxane or prostacyclin synthesis did not change after a diet rich in stearic acid.16
In mixed diets, trans-FAs are mainly substituted for saturated FAs, not for liquid oils. The purpose of our study was therefore to compare the atherogenic and thrombogenic properties of stearic acid and trans-monounsaturated FAs in a strictly controlled way in healthy subjects. The results on lipids and lipoproteins17 as well as coagulation and fibrinolysis factors18 have been published previously. This article discusses the effects of stearic acid and trans-FAs, especially those on platelet function, as measured by several in vivo and in vitro parameters as well as those on endothelial cell PGI2 production.
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Methods |
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Subjects
Altogether 80 healthy volunteers, 49 female and 31 male, entered the study after giving their informed consent. Of the female participants, one was postmenopausal. The baseline characteristics of the subjects are indicated in Table 1
.
The subjects were screened 1 month before the start of the study.
Exclusion criteria were serum cholesterol >7.0
mmol/L, hypertension, anemia, glycosuria, and proteinuria. Nineteen
women used oral contraceptives and one man smoked throughout the study.
The subjects were asked to keep their smoking habits, alcohol
consumption, and physical activity unchanged. They were also advised to
refrain from ingestion of aspirin and other anti-inflammatory drugs
known to affect platelet function 2 weeks before blood sampling.
Other than free food, the subjects received no payment.
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Study Design
The study protocol was approved by the ethics committees of the
University of Helsinki and the National Public Health Institute,
Helsinki, Finland. The participants were unaware of the diets, and the
results of biochemical determinations were not available to the
participants before the end of the study. In addition, the laboratory
staff was blinded to the subjects' group assignments. During the first
5 weeks of the study, all subjects received a baseline diet rich in
saturated FAs, mainly from dairy fat. Thereafter, the subjects were
allocated pairwise to either of two groups in the order of their serum
cholesterol values: 40 subjects (24 female, 16 male) had a
trans-FA diet and the other 40 subjects (25 female, 15
male) a stearic acid diet in a parallel manner for another 5 weeks. On
weekdays the subjects had lunch on the university premises and received
the food for the rest of the day and the next morning. Food for the
whole weekend was provided on Fridays. All food was weighed for each
participant. The subjects were weighed twice weekly, and energy intake
was adjusted when necessary to avoid weight changes.
Diets
The three diets were designed to comprise similar proportions of
energy from fats (33% of energy), carbohydrate (51% of energy ), and
protein (16% of energy); similar proportions of
cis-monounsaturated FAs and
polyunsaturated FAs; and similar amounts of cholesterol.
The diets differed only with respect to the composition of saturated
and trans-FAs. The stearic acid and
trans-FA diets contained 
9% of energy as these FAs.
Mixed solid foods customary in the Finnish diet were used in the
experimental diets, covering about 90% of the energy intake per day.
In addition to the food supplied, the subjects were allowed to freely
choose 10% of their daily energy intake from foods that were free from
fat and cholesterol (candies, fruit, beer, etc). The
subjects recorded these foods and the consumption of alcohol in
their diaries. They also recorded any signs of illness and use
of medicines.
Duplicate portions of each diet were collected daily for 1 week in the kitchen by the personnel, pooled for each diet, and analyzed. The analyzed values and those calculated for the free-choice foods were combined, giving the final composition of the diets. The fat in the baseline diet was mainly dairy fat, whereas the trans-FA and stearic acid diets were made up by using special margarines provided by Unilever Research Laboratorium, Vlaardingen, the Netherlands. The fats were used on bread and in bakery products, desserts, and cooking. The margarine high in trans-FAs was produced by partial hydrogenation of high–oleic acid sunflower oil.19 trans-monoenoic FAs were composed of 35% n-10 to n-12 isomers, 22% n-9 (elaidic acid), 19% n-8, 12% n-7, 7% n-6, 5% n-5, and <1% n-4. The margarine high in stearic acid was an inter-esterified mixture of fully hydrogenated high–linoleic-acid sunflower oil and unhydrogenated high–linoleic acid and high–oleic acid sunflower oils.19
Blood and Urine Sampling
Venous blood samples were collected with minimal stasis from
fasting (12-hour) subjects in the morning between 7:30 and 9:30
AM twice during the last week of each diet period.
Siliconized, evacuated tubes and 20-gauge needles were used. The first
10 mL of blood was used for lipid analyses and the following
tubes for platelet FA and platelet aggregation studies. The two
samples from each diet period were pooled for analysis of
platelet total and phospholipid fraction FA analysis.
Platelet aggregation measurements were done from both samples.
At the end of each diet period, the subjects also collected three consecutive 24-hour urine samples in an aliquot cup (K.K. Izumi Seisakusyo Co Ltd). During the collection period the samples were kept refrigerated, and thereafter they were rapidly frozen. Samples from women having their menstruation periods were excluded. The results of all urinary parameters were corrected for creatinine.
Platelet FA Analysis
For the measurement of platelet total and phospholipid
fraction FAs, 15 mL of blood was drawn on the same 2 days that samples
for platelet aggregation and TXB2
measurements were taken. PRP was separated and centrifuged for
10 minutes at 1000g, and the platelet pellet was
resuspended in 1 mL washing buffer (ACD/saline, 15/85 wt%/wt%, pH
7.4).20 The samples were kept frozen at -70°C
until analyzed. After the platelet pellets were thawed they
were washed twice with buffer, and the two samples from each period
were combined to yield the platelets from 30 mL of blood for
extraction.
Total lipids were extracted and methylated as described previously.21 22 Phospholipid fractions were separated from the samples of 20 subjects by thin-layer chromatography on precoated silica gel sheets. The chromatograms were developed in a solvent system of chloroform/methanol/acetic acid/water (25:15:4:2, vol/vol/vol/vol). Authentic standards were run on separate lanes. The FA methyl esters were analyzed using a Hewlett-Packard 5890 series II capillary gas chromatograph with a fused-silica capillary column (NB-351, Nordion). The oven temperature was programmed from 170°C to 230°C at a rate of 15°C/min. The amounts of individual FAs were expressed as relative percentages of the total FAs. An FA standard (Nu Chek Prep Inc) was run each day.
Platelet TXB2 and Urinary
2,3-Dinor-TXB2 Measurements
The platelet in vitro production of
TXB2 and urinary
2,3-dinor-TXB2 were measured by EIA after sample
purification.23 After purification the three
urine samples from each subject from each diet period were pooled for
analysis of 2,3-dinor-TXB2, and EIA
analysis was done from the pooled samples.
EIA Analysis
After purification the metabolites were measured by the
solid-phase EIA method of Pradelles et al24 as
described previously.25 Canine polyclonal
TXB2 antiserum produced in our laboratory was
used. All samples from each subject were analyzed in duplicate
on the same plate. For the platelet TXB2
analysis, the intra-assay and interassay coefficients of
variation were 8.7% and 11.9%, respectively, and for the urinary
2,3-dinor-TXB2 analysis, 6.7% and
14.0%, respectively.
Measurement of Urinary 2,3-Dinor-6-Keto-PGF1
Because of the expensive and time-consuming methodology, urine
samples from only 24 subjects were analyzed. Urinary
2,3-dinor-6-keto-PGF1 was analyzed
from pooled 24-hour samples collected on 3 days by combined capillary
gas chromatography/mass spectrometry as described
previously.26 The trideuterated standard
([2H3]-2,3-dinor-6-keto-PGF1)
was purchased from Biomol.
Platelet Aggregation Studies
Blood for platelet aggregation studies was drawn, and PRP
was prepared as described earlier.27
Platelets in PRP were adjusted to 250x106/mL
with autologous platelet-poor plasma, and the adjusted samples were
kept at room temperature until aggregations were performed.
Platelet aggregation was measured with the turbidimetric method of
Born28 within 2 hours of venipuncture
with an Aggre- corder IIPA-3220 aggregometer (Kyoto Daiichi Kagaku
Co Ltd). The aggregating agents used were ADP (final concentrations,
0.5, 1.0, and 2.0 µmol/L PRP; Boehringer Mannheim) and
collagen (final concentrations, 0.5, 1.0, 2.0, and 20 µg/mL PRP;
Hormon Chemie). The ADP aggregations were followed for 3 minutes and
the collagen aggregations for 5 minutes. The rate of aggregation was
indicated as the steepest slope of the aggregation curve, as calculated
by the aggregometer program (percent aggregation per minute). Samples
for TX measurements were taken after exactly 5 minutes from those in
the cuvette aggregated by collagen (2.0 and 20 µg/mL), added to tubes
containing 50 mmol/L Tris-HCl buffer (pH 7,4), immediately frozen
in liquid N2, and stored at -40°C.
Measurement of Urinary ß-TG
For each participant, the three urine samples collected at
the end of the diet periods and stored at -20°C were pooled after
thawing to yield one sample for each period. HMW ß-TG (which
presumably contains intact ß-TG) was separated from
low-molecular-weight ß-TG (ie, ß-TG fragments and/or nonspecific
interfering compounds) on Sephadex G-25M columns (Pharmacia Fine
Chemicals).29 Selective analysis of HMW
ß-TG in urine circumvents problems with nonspecific immunoreactivity
and apparent interference with measurements of intact ß-TG. HMW
ß-TG was analyzed by a commercially available
radioimmunoassay kit for ß-TG (IM-88, Amersham). Some modifications
in using the kit were done according to the method of Hjemdahl et
al29 to increase sensitivity. The intra-assay and
interassay variabilities for this method were 4.3% and 9.5%,
respectively.
Statistical Analysis
There were no overall sex differences in the results, and thus
the data were combined. The data for baseline characteristics were
analyzed with the unpaired t test. Differences
between experimental diets were analyzed with the general
linear models procedure of the Systat 5.2
program30 using treatment and baseline values as
covariates. The differences in the effects of the experimental diets on
platelet aggregation results were calculated by using a nonlinear
model of the BMDP program (version 5) including all
concentrations of the aggregating agents. Values for
2,3-dinor-TXB2 and 2,3-dinor-6-keto
PGF1 were logarithmically transformed before
testing. Correlation analysis was performed using Pearson
correlation tests. Differences with P<.05 were considered
significant.
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Results |
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Diets and Dietary Adherence
All of the subjects successfully completed the study. The subjects were weighed twice a week throughout the study, and their weights remained unchanged in both diet groups. The mean daily intake of energy and nutrients is shown in Table 2
. The
intakes of protein, fat, carbohydrate, and cholesterol were
similar in all diets, as were the intakes of polyunsaturated FAs, oleic
acid, and the sum of saturated and trans-FAs. The
stearic acid and trans-FA diets contained 9.3 energy%
and 8.7 energy% as stearic acid and
monounsaturated trans-FA,
respectively, whereas the baseline and stearic acid diets only
contained <1 energy% of trans-FA.
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Dietary compliance, as evaluated by the plasma FA profile, was good.17 During the stearic acid diet, the proportion of stearic acid increased and those of myristic, palmitic, and palmitoleic acids decreased correspondingly. Respectively, the change from the baseline diet to the trans-FA diet increased the proportion of trans-FA sevenfold.
Platelet FAs
In total platelet FAs, a significant difference between the
trans-FA and stearic acid diets was found in the
proportions of palmitic, palmitoleic, stearic, oleic, and
arachidonic acids (Table 3). Our gas
chromatography column does not separate
trans- from cis-monoenes, and they
coeluted with oleic acid. Although the proportions of oleic acid of the
baseline and trans-FA diets were practically the same,
a highly significant increase in the oleic+trans-
fraction after the trans-FA diet
(P<.001)was observed, indicating incorporation of
trans-FAs into platelet phospholipids. The
proportion of stearic acid in platelets was significantly increased
after the stearic acid diet (P=.02). Of special interest
were the effects of the experimental diets on the proportion of
arachidonic acid (C20:4.) No change was found after the
stearic acid diet, whereas the trans-FA diet decreased
platelet arachidonic acid significantly. There were
no significant changes in the proportions of longer-chain FAs (C20:5
and C22:6).
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Results for the two main platelet phospholipid fractions, PC and
PE, are presented in Tables 4 and 5. Dietary trans-FAs were
mainly incorporated into the PE fraction, as the proportion of
oleic+trans-FAs was significantly higher after the
trans-FA diet than the stearic acid diet
(P=.03), whereas the proportions of stearic acid and
palmitic acid significantly increased (P=.004 and
P=.0002, respectively) in the PC fraction after the stearic
acid diet. A strong tendency for arachidonic acid to
decrease in PE and increase in PC after the stearic acid diet was
noted.
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Platelet Function In Vivo
No difference between the stearic acid and trans-FA
diets was seen in the urinary excretion of
2,3-dinor-TXB2 (Table 6). To find out whether the use of oral
contraceptives had any effect on the results, the data were
analyzed separately for those women using oral contraceptives
and those who were not. In the users no change was observed in the
excretion of 2,3-dinor-TXB2 when they were
switched from the baseline to the trans-FA diet (1076
versus 1058 pg/mg creatinine), whereas in the
nonusers excretion of this metabolite was significantly
increased (931 versus 1455 pg/mg creatinine). The
difference between users and nonusers was significant
(P=.03).
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The effects of the experimental diets on the excretion of the urinary
metabolite of PGI2 were also similar (Table 6
).
The TX-to-PG ratio was similarly affected by both diets as well: the
ratio was 9.2 during the saturated baseline diet and 12.8 after the
stearic acid diet, and 5.8 and 11.1 on the baseline and the
trans-FA diets, respectively.
Urinary ß-TG was analyzed from pooled 24-hour urine samples
collected on 3 days. The average excretion rates after the baseline and
stearic acid diets were 25.3 and 26.6 pg/mL, respectively, and 19.9 and
19.1 pg/mL after the baseline and trans-FA diets,
respectively (Table 7). The differences
between the diet responses were not significant.
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Platelet Function In Vitro
Platelet aggregation was measured from two samples taken 4
days apart at the end of each diet period, thus minimizing the effect
of day-to-day variation in platelet reactivity on the possible
differences between the diets. ADP-induced aggregation was decreased
after the trans-FA diet, whereas collagen-induced
aggregation was enhanced after the stearic acid diet (Table 7). The
difference between the effects of the stearic acid and
trans-FA diets was calculated using a linear model in
which all concentrations of the aggregating agent were included and was
significant for collagen (P=.02) but not for ADP
(P=.17)(Table 7).
The capacity of platelets to produce TXB2
during in vitro stimulation was studied with two concentrations of
collagen: 2 and 20 µg/mL. Although both concentrations caused maximal
platelet aggregation, production of
TXB2 was more than threefold higher at 20 µg/mL
(65 versus 18 ng/mL), but no significant differences between the
stearic acid and trans-FA diets were found for either
concentration (Table 7).
Correlation Analysis
Excretion of 2,3-dinor-TXB2 was not
correlated with changes in platelet total FAs, platelet
aggregation, TXB2 production, or urinary
ß-TG excretion, nor with the excretion of the corresponding
metabolite of PGI2,
2,3-dinor-6-keto-PGF1. Urinary ß-TG was not
correlated with in vitro aggregation due to ADP or collagen, urinary
excretion of 2,3-dinor-TXB2, or changes in
platelet total FAs. In both the stearic acid and
trans-FA groups, collagen aggregation was significantly
correlated with TXB2 production at a
concentration of 20 µg/mL (P=.007 to .03), but not at 2
µg/mL (P=.143 to .615). Collagen aggregation was also
significantly correlated with total platelet
arachidonic acid content (r=0.4,
P=.03) after the trans-FA diet, but there
were no significant correlations between arachidonic
acid and aggregation results after the stearic acid diet.
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Discussion |
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The effects on lipoprotein metabolism of trans--FAs (compared with cis-unsaturated FAs)1 2 31 and stearic acid10 11 32 have been studied frequently, but very little is known of the other properties, ie, thrombogenicity, of these FAs concerning CHD risk. Therefore, we compared the short-term effects of stearic acid and elaidic acid, the main monounsaturated trans-FA in Western diets, on several parameters of platelet function in a strictly controlled dietary intervention. According to the analyzed composition of the pooled duplicate diets, intakes of cis-monounsaturated and polyunsaturated FAs were similar for all three diets, and the only changes were within saturated and trans-FAs. Also, the weight of the subjects remained stable. The results obtained may therefore be attributed to dietary FA composition. However, the design of the study only allows for comparison between the stearic acid and trans-FA diets.
The results for both in vivo parameters of platelet activation, ß-TG and 2,3-dinor-TXB2; in vitro TXB2 production; and ADP-induced aggregation, as well as production of endothelial PGI2, all showed similar effects of the stearic acid and trans-FA diets. Only collagen aggregation was significantly different between the diets and was supported by a difference in arachidonic acid in total platelet phospholipids.
In the few human studies in which in vivo parameters of platelet activation have been measured, usually no changes or differences between diets have been found as a result of dietary manipulation. Excretion of 2,3-dinor-TXB2, seen to reflect systemic TXA2 production,33 is the result of a complicated interplay of enzymes, membrane properties, receptor activities, etc affecting the release of arachidonic acid from platelet membrane phospholipids. Differences at one stage of the cascade may be masked by differences at another stage, and thus, the possibility of differences during the process cannot be excluded, although the end result was similar. In the case of ß-TG, a platelet-specific protein released during platelet granule secretion, it may be that baseline urinary excretion is not affected, even with marked dietary manipulation. Fish oil or linseed oil supplementation did not affect urinary ß-TG excretion differently in healthy subjects in a study by our group,34 nor were any changes found in plasma ß-TG after diets rich in partially hydrogenated fish oil, partially hydrogenated soybean oil, or butter fat,35 although in disease states associated with increased platelet activation (such as diabetes mellitus,36 deep vein thrombosis,37 and coronary artery disease38 ) elevated plasma or urinary levels have been found.
In vitro measurements are criticized for the "unphysiological" environment in which they are performed. However, it may actually give a better picture of the changes in platelets, when the possible contribution of erythrocytes and leukocytes, for example, is excluded. The collagen results of the present study, supported by platelet FA data, suggest that stearic acid and monounsaturated trans-FAs have different effects on platelet aggregability. What this difference means or what the mechanism of action is remains to be resolved. Altered membrane properties could be a consequence of the trans-FA diet in particular, which presumably increases membrane rigidity. This in turn could lead to an impairment in receptor function or spontaneous or enhanced liberation of arachidonic acid, which could thus provoke platelet activation, possibly explaining our in vitro versus in vivo differences. The fact that collagen-induced aggregation and in vitro TX production did not show correlations as they did in several other studies39 40 may be explained by the concentrations used to induce TXB2 production, which were beyond concentrations that cause maximal aggregation and are far from physiological.
In healthy subjects the urinary excretion of PGI2 and TX metabolites is normally low. The effects of dietary changes on endothelial function, especially PGI2 production by vascular endothelial cells, are largely unknown at present. It is unclear whether PGI2 production can be modified by the intake of saturated or monounsaturated FAs,16 41 42 43 whereas the consumption of fish or fish oil has been shown to increase the urinary excretion of PGI3.44 45 In the present study, PGI2 excretion levels and TX-PG ratios were similar for the stearic acid and trans-FA diets and do not indicate differences in endothelial function between these FAs .
Comparisons with baseline/background diets are not statistically justified in parallel studies without a control group. Especially in a supplementation study, several uncontrolled factors may cause a drift in time. However, in a strictly monitored intervention wherein both weight and food intake are controlled, the risk of any drifts is significantly smaller. In the present study, some conclusions may thus be drawn when comparing the stearic acid and trans-FA diets with the baseline dairy fat diet. Both experimental diets seemed to increase the excretion of urinary 2,3-dinor-TXB2 as well as the TX-PG ratio. Excretion of PGI2 metabolites decreased after the trans-FA diet, while in general, the endothelial response to the diets was a magnitude weaker than that in platelets. On the basis of these observations, it is possible that the experimental diets may have an unfavorable effect on the TX-PG balance when compared with the dairy fat diet.
Previously the effects of stearic acid and monounsaturated trans-FAs on platelets have not been compared in humans. Also, other studies involving stearic acid or trans-FAs and platelets are few. Hornstra14 studied the prothrombotic effect of individual FAs in rats ex vivo by using the aorta-loop method. He showed that dietary fats rich in long-chain saturated FAs promote arterial thrombogenesis, whereas monounsaturated FAs are neutral and decrease arterial thrombosis tendency only when they replace long-chain saturated FAs. No difference between the antithrombotic effect of cis-FAs and their trans- isomers was found, the result being in line with ours.
No significant changes were found in the urinary excretion of TX or PGI2 metabolites or the TX-PG ratio in healthy males after they consumed diets high or low in stearic acid (7.3 versus 1.6 energy%).16 Mustad et al41 were also unable to show differences in urinary TXB2 between diets rich in stearic acid and those rich in lauric and myristic acids, although the stearic acid diet significantly decreased platelet arachidonic acid. A significantly smaller mean platelet volume was found after a stearic acid–rich diet (8 energy%) than after a palmitic acid diet in a controlled human study, indicating a more disc-like, less-activated state for the platelets in vivo. This was further confirmed by a significantly greater increase in mean platelet volume after the stearic acid diet in response to added ADP, again suggesting an initially less-activated state for platelets after this diet.46
The amounts of trans-FAs (8.7 energy%) used in this study are high compared with the average intake of 1 to 5 energy% in different countries47 48 but may be achieved by some groups of individuals in high-intake countries, eg, Canada (B. Holub. personal communication, 1997). Our study shows that stearic acid and trans-FAs are well incorporated into platelets but do not seem to differ in their effects on platelet activation, as measured by several in vivo and in vitro parameters representing different aspects of platelet activation. The results of in vitro collagen-induced aggregation, supported by platelet FA data, illustrate on the other hand, differential properties for these FAs. The results also emphasize the need to use complementary methods to assess platelet function, not only the in vitro platelet aggregation test that is generally used. Further research on cell signaling pathways and signal transduction with these FAs could possibly give further information on the in vivo situation and mechanisms of action of these and other dietary FAs.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by grants from the Unilever Research Laboratorium, Vlaardingen, the Academy of Finland, the Finnish Cultural Foundation, the Food Research Foundation, and the Yrjö Jahnsson Foundation. The authors are grateful to the subjects for their cooperation, Sirkka-Liisa Sarpola for technical assistance, and Pertti Mutanen, MSc, for statistical advice. Some of the foods were kindly supplied by the Finnish food industry.
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Footnotes |
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Reprint requests to Anu M. Turpeinen, Department of Applied Chemistry and Microbiology, Division of Nutrition, Latokartanonkaari 7, PO Box 27, 00014 University of Helsinki, 00710, Helsinki, Finland.
Received March 13, 1997; accepted November 12, 1997.
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