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© 1996 American Heart Association, Inc.
Articles |
Monounsaturated Fatty Acid–Enriched Diet Decreases Plasma Plasminogen Activator Inhibitor Type 1
From Unidad de Lípidos y Arteriosclerosis (F.L.-S., J.L.-M., P.C., A.B., J.J.-P., J.T., F.P.-J.), Servicio Hematologia (F.V., R.L.-P., A.T.), Hospital Universitario Reina Sofia, Córdoba, Spain, and Lipid Metabolism Laboratory, USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Mass (J.M.O.).
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Abstract An increase in levels of plasma plasminogen activator inhibitor type 1 (PAI-1) is one of the main hemostatic alterations in patients with coronary heart disease. Despite growing interest in the fibrinolytic system, few studies have been undertaken to determine the effect exerted on it by the different dietary fatty acids. We investigated the effect of a monounsaturated fat (MUFA)–rich diet in comparison with a low-fat diet (National Cholesterol Education Program step 1 diet) (NCEP-1) on factors involved in blood coagulation and fibrinolysis. We also determined the effect of dietary cholesterol on these blood parameters. Twenty-one young, male, healthy volunteers followed two low-fat/high-carbohydrate diets (<30% fat, <10% saturated fat, 14% MUFA) for 24 days each, with 115 or 280 mg of cholesterol per 1000 kcal per day, and two oleic acid–enriched diets (38% fat, 24% MUFA) with the same dietary cholesterol as the low-fat/high-carbohydrate diets. Plasma levels of fibrinogen, thrombin-antithrombin complexes, prothrombin fragments 1+2, plasminogen,
2
antiplasmin, and tissue plasminogen activator
were not significantly different among the experimental diets used in
this study. Consumption of the diet rich in MUFA resulted in a
significant decrease in both PAI-1 plasma activity (P<.005)
and antigenic PAI-1 (P<.04) compared with the
carbohydrate-rich diet (NCEP-1). The addition of dietary
cholesterol to each of these diets did not result in any
significant additional effect. Changes in insulin levels and PAI-1
activity were positively correlated (r=.425;
P<.02). In conclusion, consumption of diets rich in MUFAs
decreases PAI-1 plasma activity, which is accompanied by a parallel
decrease in plasma insulin levels.
Key Words: low-fat diets • monounsaturated fatty acid–rich diets • plasminogen activator inhibitor type 1 • insulin • fibrinolytic system
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Formation of fibrin thrombi on atherosclerotic plaques is a determining factor in the growth of atherosclerotic lesions and the appearance of clinical manifestations.1 2 It has been demonstrated that fibrin stimulates smooth muscle cell proliferation3 and LDL accumulation in lesions.4 This implies that decreased fibrinolytic activity would lead to decreased destruction of fibrin deposits, which in turn would favor atherothrombosis. The principal physiological inhibitor of fibrinolysis is PAI-1, a natural inhibitor of TPA and urokinase-type plasminogen activator.5 Several clinical studies have suggested that increased levels of PAI-1 or TPA antigen (which mainly represents inactive TPA/PAI-1 complexes) constitute a risk factor for CHD.6 7 8 Also, PAI-1 levels have been shown to be closely correlated with TPA antigen and with several coronary atherosclerotic risk factors, such as insulin,9 10 BMI,10 triglycerides,10 and systolic arterial blood pressure.11 PAI-1 thus could play an important role in the pathogenesis of atherosclerosis. Furthermore, recent results from a prospective multicenter study12 including 3043 patients with angina pectoris who underwent coronary angiography demonstrate that after a 2-year follow-up, levels of fibrinogen, von Willebrand factor antigen, and TPA antigen were independent predictors of subsequent acute coronary syndromes.
High intake of SAT has been associated with an increased incidence of CHD, whereas high intake of MUFAs has been associated with a protective effect.13 14 One of the mechanisms by which dietary fats can modify CHD risk is by their effect on plasma LDL and HDL cholesterol levels.15 In addition, other non–lipid-related mechanisms may also be affected by dietary fat. Few studies have been carried out to determine the influence of these dietary factors on blood coagulation and fibrinolysis, and most of the emphasis has been on the effect of n-3 PUFAs16 17 18 or high-carbohydrate diets.19 Less information is available on the influence of MUFAs,20 21 a major component in the diet of Mediterranean countries, on these variables.
Western societies are becoming increasingly aware of the need to lower plasma cholesterol levels to decrease the high prevalence of CHD. To achieve this reduction, current recommendations for the general population are to limit dietary fat to <30% of calories, SAT to <10%, and cholesterol to <300 mg/day (NCEP-1 diet).22 In addition to its effect on lipoproteins, a low-fat/high-fiber diet may have a beneficial effect on the fibrinolytic system.19 The main objective of this study was to determine the effect of a MUFA-rich diet in comparison with a low-fat diet (NCEP-1) on factors involved in blood coagulation and fibrinolysis. We also determined the effect of dietary cholesterol on these blood parameters.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Subjects and Protocol
Twenty-two healthy male subjects (mean age, 23.4±5.6 years) were enrolled in the study. The subjects were students. Complete medical examination and routine laboratory tests were performed for all subjects to assess their health status. Plasma cholesterol levels at the time of screening were <5.7 mmol/L. None of the subjects were taking any medication or dietary supplements. Mean BMI (weight [kg]/height[m]2) was 24.7±3.7 (mean±SD) and did not change significantly (>1%) during the experimental period. Information on daily physical activity and a 7-day dietary record were elicited from each subject to calculate individual caloric requirements. Informed consent was obtained from all participants. This protocol was approved by the Human Review Committee at the Reina Sofia University Hospital.
The study design (Fig 1
) included
an initial 24-day
period during which all subjects consumed an NCEP-1 diet calculated to
provide <30% of total calories from fat, with <10% SAT, 14% MUFA,
and 6% PUFAs, with 115 mg of cholesterol per 1000 kcal per
day. After this period, two groups of 11 subjects each were assigned to
one of two dietary regimens in a randomized, crossover design for two
24-day periods. Group 1 was placed on a high-fat diet (38% fat)
containing 22% MUFA (olive oil) and 115 mg of cholesterol
per 1000 kcal for 24 days (MUFA diet), followed by a 24-day diet of the
same fat composition but containing 290 mg of cholesterol
per 1000 kcal (MUFACHOL diet). Cholesterol enrichment was
provided by two eggs per day. Both diets contained 17% protein, 45%
carbohydrate, and 38% fat (SAT 10%, PUFA 6%, and MUFA 22%). The
order of the diets for individuals in group two was reversed.
Assignment of volunteers to the sequence of diets was random.
Afterward, an NCEP-1 dietary period was implemented with a
cholesterol content of 290 mg per 1000 kcal over a period
of 24 days (NCEPCHOL diet). Caloric intake was adjusted as required to
maintain initial body weight. Body weight was controlled by taking
measurements twice each week; overall change throughout the diet
intervention periods was 0.3±0.5 kg. Two investigators supervised the
feeding of the subjects and were blinded to the changes in serum
chemistry values. The other investigators supervised or performed all
laboratory analyses and were blinded to the dietary
assignments. The study was conducted during the first few months of
1993. One subject was excluded from the study because he suffered an
acute illness during one diet period.
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Diets
The composition of the experimental diets was
calculated by use
of the USDA food composition tables or the Spanish food composition
tables for certain local foodstuffs. Fourteen menus of conventional
mixed solid foods were rotated during the different days of the week.
These included fish, veal, pork, chicken, ham, cheese, legumes, rice,
pasta, and vegetables. In addition, subjects consumed a fixed amount of
fruit, bread, jam, whole milk, and green salad daily. Virgin olive oil
(Olea Europea, provided by Koype Company), crude and unrefined, was
used for cooking, for salad dressing, and for toast in the MUFA diet
period. Fish intake was the same in the low- and high-fat diet
periods. In the NCEP-1 diet, olive oil was replaced by cookies, bread,
and marmalade.
All meals were cooked and consumed in the school canteen. Duplicate food samples from each diet period were collected, homogenized, and stored at -70°C. Homogenates were analyzed for dietary protein, fat, and carbohydrates by standard methods.
Blood Sampling and Biochemical Determinations
Blood samples
for hemostatic variables were obtained by
venous puncture after a 12-hour fasting period and were pooled in tubes
containing 3.8% sodium citrate in a 1:9 proportion. Blood for lipid
and lipoprotein analysis was collected into tubes containing
EDTA. Sample collection was always carried out at 9 AM to
minimize circadian variations in fibrinolytic variables.
Platelet-poor plasma was obtained by
centrifugation at 4°C for 15 minutes at
3000g. All analyses were performed at the end of the
study on samples stored at -70°C, to minimize the variability
of the assay.
Fibrinogen was assayed by the method of Clauss with the
Ortho
quantitative fibrinogen assay in an automated Koagulab 60-S
Coagulometer (Ortho-Diagnostic).23 The TAT
complex was determined by use of an enzyme immunoassay with an Enzynost
TAT Kit (Behringwerke AG).24 Prothrombin fragments 1+2
were determined by use of an enzyme immunoassay with an Enzynost F1+2
micro kit (Berhingwerke AG).25 Plasminogen was
determined by chromogenic substrates according to the
method of Friberger et al.26 2 Antiplasmin
was determined by chromogenic substrates with a Coatest
antiplasmin Kit (Kabi).27 The results of
plasminogen and 2 antiplasmin are expressed
as a percentage of pooled plasma from 20 donors. TPA antigen was
measured by Asserachrom ELISA Kit
(Diagnostica).28 Antigenic PAI-1 was
quantified by an enzyme immunoassay to determine human PAI-1 antigen
with a TintElize-PAI-1 Kit (Biopool).29 PAI-1 activity was
quantified by a chromogenic assay for determination of
PAI-1 activity with a Spectrolyse/Fibrin PAI Kit
(Biopool).30 All analyses were performed at the
end of the study in one run for each individual on samples stored at
-70°C, to minimize the variability of the assay.
The quantitative determination of insulin levels was made by radioimmunoassay31 with a commercial kit (125I-Insulin Coatria, BioMerieux). The intraassay coefficient of variation for insulin was 5.6%.
We separated plasma VLDL, LDL, and HDL by ultracentrifugation.32 Cholesterol and triglycerides in plasma and lipoprotein fractions were assayed by enzymatic procedures.33 34 Apolipoprotein A-I and B concentrations were determined by turbidimetry.35 The fatty acid pattern in LDL cholesterol esters was determined at the end of each dietary period as described previously.36
Statistical Analysis
Data were analyzed with CSS (Statsof,
Inc). Because of
skewed distributions of most variables, nonparametric
statistics were applied. Friedman ANOVA and Wilcoxon
matched-pairs signed-rank tests were used for comparison of the
four diets. Correlation analysis was performed with Spearman's
rank correlation. A value of P<.05 was considered
significant. All data are presented in the text and tables as
either median and 95% confidence intervals or mean±SD.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Age, BMI, and plasma lipid levels of the 21 subjects who completed the study are shown in Table 1
. Diet composition was
analyzed in duplicate meal portions, and results are shown in
Table 2. These results were in good agreement with
values obtained from the food composition tables. Fatty acid
composition was analyzed during each diet period on the
cholesterol ester fraction of plasma LDL (Table 3). Enrichment
in oleic acid was observed during the
high-MUFA diet period, suggesting good adherence to the diet
protocol.
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Plasma levels of fibrinogen, TAT complexes, prothrombin fragment 1+2,
plasminogen, 2 antiplasmin, and TPA plasma
levels were not significantly different among the different
experimental diets used in this study (Table 4).
However, consumption of the diet rich in MUFA resulted in a significant
decrease (P<.005) in PAI-1 plasma activity compared with
the carbohydrate-rich diet (NCEP-1). The addition of dietary
cholesterol to each of these diets did not result in any
significant additional effect (Table 4 and Fig
2).
Similarly, antigenic PAI-1 plasma levels also decreased
(P<.04) after administration of both MUFA-rich diets (Table
4).
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Significantly different from
NCEPCHOL diet (P<.01).
Fasting plasma insulin levels significantly decreased at the end of
both dietary periods rich in MUFAs compared with carbohydrate-rich
diets (Table 4
). Changes in insulin levels and PAI-1 were
positively
correlated (r=.425; P<.02). Moreover, the
decrease in PAI-1 was greater in the high tertiles of insulin decrease
(P<.003) (Fig 3).
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Plasma lipid and lipoprotein fractions at the end of each diet period
are presented in Table 5. No statistically
significant differences were observed for any of the lipid
variables determined between the NCEP-1 and the MUFA diet periods.
The addition of dietary cholesterol to the NCEP-1 diet
resulted in a significant increase in total plasma
cholesterol levels (3.72±0.65 versus 4.11±0.62 mmol/L;
P=.001), primarily due to an increase in HDL
cholesterol levels (1.19±0.34 versus 1.34±0.31 mmol/L;
P=.04). The addition of cholesterol to the
high-MUFA diet resulted in a significant increase in total plasma
cholesterol levels (3.75±0.59 versus 4.01±0.57 mmol/L;
P=.024), which in this case was primarily due to a
significant increase in LDL cholesterol level (2.07±0.49
versus 2.33±0.57 mmol/L; P=.009). Plasma and VLDL
triglycerides were not significantly affected by dietary
treatment (Table 5). In these
normotriglyceridemic subjects, no correlation
was noted between total plasma or VLDL triglyceride levels
and PAI-1 plasma levels or antigenic activity (data not shown).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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An increase in plasma PAI-1 levels is one of the main hemostatic alterations of patients with CHD, especially those with acute myocardial infarction or angina.5 6 PAI-1 activity has also been shown to increase in atherosclerotic arterial walls,37 suggesting that both systemic and local concentrations could play a pathogenic role in the development of atherosclerotic disease.
Despite growing interest in the fibrinolytic system, few studies have been undertaken to determine the effect exerted on it by different dietary fatty acids. Previous studies have shown that fat intake has no short-term inhibitory effects on the fibrinolytic system and induces an activation of coagulation factor VII.38 39 40 41 Several studies have indicated that low-fat/high-fiber diets may cause a decrease in factor VII coagulant activity.42 43 44 Marckmann et al19 showed that prolonged administration of a carbohydrate- and fiber-rich diet increased TPA-dependent fibrinolytic activity compared with a diet rich in SAT, although they did not observe, by antigenic methods, changes in TPA and PAI-1 plasma levels. Administration of a diet rich in n-3 PUFAs caused an increase in plasma PAI-1 both in healthy individuals16 17 18 45 and in diabetics.46 The effect of diets rich in MUFA on the components of the fibrinolytic system is still unknown.
The present study shows that after consumption of MUFA-rich diets by healthy young men for 24 days, both PAI-1 plasma concentration and activity were significantly lower compared with the period in which the subjects consumed a low-fat, carbohydrate-rich diet; however, because of the fact that our design did not include a crossover period between the high-fat and NCEP diet periods, we cannot eliminate the possibility of some period effect. Nevertheless, in previous studies, we did not detect such effects with regard to plasma lipid variables.47 No dietary effect was demonstrated for any other component of the fibrinolytic system. Increased levels of dietary cholesterol did not have any significant effect on the variables examined. Previous studies in rats revealed that an increase in dietary fat content or changing dietary fatty acid composition had no effect on PAI-1 plasma activity.21 This divergence from our results probably stems from an interspecific difference in the fibrinolytic system. With respect to this, it is worth noting that rats differ from humans in several aspects related to PAI-1 synthesis. In rats, hepatic synthesis of PAI-1 occurs predominantly in the endothelial cells of hepatic sinusoids;48 in humans, however, the hepatocytes also produce PAI-1.49 Another important difference is that in humans, PAI-1 is responsible for almost 70% of the plasma inhibitory activity of the plasminogen activator,16 whereas in rats, this figure is only 40%,50 with the remaining fraction due to a still unknown inhibitory activity.
To date, the mechanisms involved in a MUFA-induced decrease in PAI-1 plasma activity are not known. There are, however, a number of hypotheses to take into consideration. The relations of BMI, fat distribution, and plasma triglyceride levels with PAI-110 levels has been established. It also has been shown that secretion of PAI-1 by cultured human umbilical vein endothelial cells is induced by VLDL51 and that this effect is much more marked in VLDL isolated from hypertriglyceridemic subjects. In the present study, plasma total, LDL, and HDL cholesterol levels as well as plasma and VLDL triglyceride levels were not affected by the change from a low-fat to a high-MUFA diet. As previously shown by other investigators,52 addition of cholesterol to each diet resulted in an increase in total plasma cholesterol, but no effect was observed on plasma or VLDL triglyceride levels. Since BMI, fat distribution, and plasma triglyceride levels did not change significantly in our study in the distinct dietary periods, we cannot credit those variables with the change in PAI-1 levels observed after MUFA-rich diets. Several studies have shown that PAI-1 levels are closely related to fasting insulin levels.9 10 The increase in PAI-1 levels observed in obese patients or type II diabetics is also related to increases in plasma insulin. Moreover, the relationship between plasma PAI-1 and BMI, triglycerides, and blood pressure is generally secondary to the relationship between PAI-1 and insulin.53 All of these facts imply that insulin resistance could be an important etiologic factor in the increase in PAI-1 levels. Moreover, intervention studies have shown that a reduction in the degree of insulin resistance is accompanied by a simultaneous decrease in plasma insulin, triglyceride level, and PAI-1.54 In accordance with these observations in diabetic subjects, we have also observed a direct relationship between changes in plasma PAI-1 levels and insulin in our study population, consisting of young, healthy, normolipemic male subjects. All data combined suggest a hypothetical causal relationship between these two parameters.
The mechanism by which insulin causes an increase in plasma PAI-1 is not yet clear. However, several in vitro studies showed an increase in PAI-1 production after incubating endothelial cells of arterial origin55 and hepatocellular cell line Hep G256 57 with insulin. Moreover, recent studies showed that an increase in insulin-mediated PAI-1 production in hepatocytes is due to mRNA stabilization.57
In conclusion, consumption of diets rich in MUFAs decreases PAI-1 plasma activity, which is accompanied by a parallel decrease in plasma insulin levels. This phenomenon could be involved in the lower incidence of CHD in populations that have a high oleic acid consumption, such as in the Mediterranean area, and implies that substitution of SATs in the diet for MUFAs could be preferable to their replacement by carbohydrates.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by a grant from Consejeria Agricultura y Pesca, Junta de Andalucia, and the Spanish Ministry of Health (FIS 92/0182).
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Footnotes |
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Reprint requests to Prof Francisco Pérez-Jiménez, Unidad de Lípidos y Arteriosclerosis, Hospital Universitario Reina Sofia, Avda Menendez Pidal, s/n 14004 Córdoba, Spain.
Received June 2, 1995; accepted October 20, 1995.
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