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*
Departamento de Nutrición,
Sección Departamental de Química Analítica,
**
Instituto de Nutrición y Bromatología (CSIC-UCM), Facultad de Farmacia, Universidad Complutense de Madrid, Madrid, Spain and
Nutrition and Genomics, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111
2To whom correspondence should be addressed. E-mail: frasan{at}farm.ucm.es.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • apolipoprotein AI and AII • HDL composition • high oleic acid sunflower oil • palmolein • postmenopausal • women
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–3
). Human HDL is isolated from plasma within the density range of 1.063 to 1.21 kg/L and contains 
5% triglycerides, 20% cholesterol, 25% phospholipid and 50% protein by weight with apolipoprotein (Apo) AI and Apo AII as the major protein constituents (70 and 20% of HDL protein mass, respectively) (4
). HDL are very heterogeneous and contain subpopulations that differ in lipid and protein composition and thus in density, size and functional properties (5
,6
).
CHD patients have been found to have significantly lower contents of some HDL subpopulations, containing only Apo AI, and significantly higher contents of other HDL subpopulations, containing both Apo AI and Apo AII. Those containing only Apo AI are known as lipoproteins LpAI, whereas those containing both Apos are called LpAI/AII (7
).
LpAI particles appear to play a central role in facilitating reverse cholesterol transport; thus, they have a protective role in the development of CHD (8
). Conversely, LpAI/AII particles have been related to a higher cardiovascular risk (7
), through mechanisms that may involve inhibition of lecithin cholesterol acyl transferase (LCAT) activity or impaired receptor binding (7
). Diet has been found to play a mayor role in modulating HDL cholesterol. Energy contribution from fat and the dietary fatty acid profile have been proposed as factors exerting the greatest effects on HDL cholesterol levels (9
,10
). Moreover, reduction in dietary total and saturated fat decreased both HDL2 and HDL3 cholesterol although the decrease in large HDL (HDL2 and HDL2b) was more pronounced (11
). However, very little information exists regarding the specific effects of dietary saturated or unsaturated fatty acids on Apo AII levels. Previous reports have shown conflicting results from the substitution of a diet rich in cholesterol and saturated fatty acids by others low in fat with a high ratio of polyunsaturated to saturated fatty acids (12
,13
).
The risk of CHD increases in postmenopausal women due to decreased estrogen synthesis (14
). We reported previously in postmenopausal women that saturated fatty acids increased cholesterol and LDL cholesterol compared with monounsaturated fatty acids (15
). The aim of the present study was to examine the changes in Apo AII levels in postmenopausal women resulting from more moderate changes in diet consisting of a 10% energy exchange between palmitic (from palmolein) and oleic acids (from high oleic acid sunflower oil).
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Fifteen women were enrolled in the study. They were part of a religious community with a regular lifestyle and dietary habits. One was excluded from the experiment because she was premenopausal. None of the participants had presented previous cardiovascular, metabolic or systemic diseases, or was taking any drug that might affect lipid metabolism. All subjects gave their informed consent before their inclusion in the study. The protocol was approved by the Committee for Human Studies at the Universidad Complutense de Madrid and performed in accordance with the Helsinki Declaration. Subjects were requested to maintain their normal patterns of activity, and not to add any food items to their usual meals. Some characteristics of the population are shown in Table 1
.
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Study participants were assigned to two consecutive 28-d experimental periods. In the first period, all participants consumed a diet enriched in oleic acid, using high oleic acid sunflower oil as the only culinary fat. This was followed by a second diet period rich in palmitic acid from palmolein. In a pilot study we performed in the same community, we used a crossover design (16
). However, the logistics involved in food preparation and consumption in the community prevented us from using a crossover design in this study. For example, food preparation at the kitchen of the community was too difficult and time-consuming because the same food was cooked with two oils. Furthermore, some members of the community complained because they thought that they were consuming a less healthy diet than other members. Therefore, we were concerned about the feasibility of accomplishing a full size study under those circumstances and we opted for the sequential design.
Diets.
During the two consecutive, experimental dietary periods, menus and individual rations were maintained. Experimental diets were assessed for 4 wk using the precise weighing method (17
). All ingredients used in the preparation of foods were weighed, as was the inedible wastage. The cooked weights of individual portions and table waste were also recorded. Energy and nutrient intakes were calculated using tables of food composition for the raw weights of foodstuffs (18
). Two investigators were present every day in the community’s kitchen during the preparation of meals. The only distinguishing feature of the diets was the oil used, i.e., oleic acid–rich sunflower oil (Koipe, Andújar, Spain) during the first 28-d period, and palmolein (AGRA S.A., Bilbao, Spain) during the second period. Both oils were used for cooking (for sautéing, frying and pot-roasting and the preparation of fish, egg, vegetable and other stews) and salad dressing. Because palmolein is solid at room temperature, this oil was liquefied by immersing the amount to be used in a water bath at 30°C just before use. To ensure constant consumption of palmolein from salads, subjects were advised to remove any oil remaining on their dishes using small pieces of bread. Basal and experimental diets (14-d menu) had the same energy and cholesterol contents and contained similar amounts of most of the essential nutrients (except for essential fatty acids, fat-soluble vitamins and other related compounds).
Fatty acid analysis.
Oil samples were saponified with 0.5 mol/L NaOH (40 mL/g) and then methylated with boron trifluoride by following the IUPAC method (19
). The fatty acid content of the oils was analyzed in a Hewlett-Packard 5890 Series II chromatograph (Palo Alto, CA) equipped with a 50-m (i.d., 0.22 mm) capillary column BPX70, 0.25-µm film thickness (SGE, Austin TX). The major fatty acid compositions of oleic acid–rich sunflower oil and palmolein were as follows: palmitic acid, 4.7 and 40.6%; stearic acid, 4.5 and 4.2%; oleic acid, 77.1 and 40.7%; and linoleic acid, 11.5 and 12.2%, respectively.
Blood sampling and biochemical determinations.
Blood samples were collected by venipuncture at 0830 h after a 12-h overnight fast. Serum was separated by low speed centrifugation at 1500 x g, at 4°C for 30 min within 1 h of sampling. Total cholesterol, phospholipids and triglycerides were determined in serum samples and in the HDL fraction using a Technicon RA-500 autoanalyzer (Tarrytown, NY) and standard enzymatic procedures (Boehringer Mannheim, Mannheim, Germany). Apo A-I determinations were performed by immunoturbidimetry using protocol, controls and calibrators of Technicon. Apo AII was determined by rocket immunoelectrophoresis according to of the method of Laurell (20
) with slight modification. HDL composition was studied after isolation of this lipoprotein fraction from serum by 21-h density gradient ultracentrifugation at 272,000 x g and 8°C in a Beckman L8–70M ultracentrifuge, SW-41 rotor (Palo Alto, CA), according to the method of Terpstra et al. (21
) with a slight modification as previously reported (22
). Commercially available quality controls (Precinorm reference 225053, and Precilip reference 781827 (Boehringer Mannheim) were included in all assays. Proficiency testing quality external control of Welcome Diagnostic Quality was used for Apo determinations. All intra-assay and interassay CV were <5.5%.
Statistical analysis.
The data presented in text and tables as means ± SD were analyzed by a paired Student’s test. Repeated-measures ANOVA was used to assess the oil effect in women with a total cholesterol level < 6.21 mmol/L compared with those with a total cholesterol level 
6.21 mmol/L.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Daily intakes of macronutrients and different fatty acids during basal and experimental diet periods are presented in Table 2
. Daily cholesterol intake was 400 mg. The experimental oils provided 62% of the total fat intake in both diets. Diets were normocaloric (adjusted to the individual energy requirements), with an adequate energy contribution from protein but rather high from fat and low from carbohydrates (Table 2)
. It should be noted that the usual diet of the participants in this study did not include meat or meat products and included a relatively high level of cholesterol from eggs and whole milk.
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-linolenic acids for the diet periods. During the palmolein diet period, saturated fatty acids and palmitic acid were provided mainly by the fats plus oil food group (data no shown). Lipids and lipoproteins.
The palmolein diet significantly increased serum total cholesterol (17.7%, P < 0.001), phospholipids (10.9%, P < 0.001) and Apo AII (38.0%, P < 0.001), with no effect on serum triglycerides, the total cholesterol/HDL cholesterol ratio or Apo AI (Table 3
). The Apo AII changes in individual subjects are shown in Figure 1
. Compared with the high oleic acid sunflower oil diet, the palmolein diet significantly increased the concentration of HDL cholesterol (14.9%, P < 0.05), HDL total lipids (cholesterol + triglycerides + phospholipids) (11.2%, P < 0.05), HDL total protein (5.9%, P < 0.01) and total particle mass (protein + lipids) (7.5%, P < 0.05). The HDL cholesterol/Apo AI ratio was significantly increased (17.8%, P < 0.05), whereas the HDL cholesterol/Apo AII and the Apo AI/Apo AII ratios were decreased (19.4%, P < 0.01 and 30.4%, P < 0.001, respectively) (Table 3)
.
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). The cholesterol (P < 0.05), Apo AII (P < 0.001), total protein (P < 0.01), total lipids (P < 0.05), total mass (P < 0.01), the cholesterol/Apo AI (P < 0.01), cholesterol/Apo AII (P < 0.001) and Apo AI/Apo AII (P < 0.001) ratios were significantly affected in the HDL by the oil change. Furthermore, cholesterol (P < 0.05), phospholipids (P < 0.01), Apo AI (P < 0.01), total protein (P < 0.05), total lipids (P < 0.01), total mass (P < 0.01), the cholesterol/Apo AII (P < 0.05) and Apo AI/Apo AII ratios (P < 0.05) were significantly affected in HDL by the women’s serum cholesterol concentration. A significant oil by cholesterol level interaction was found for Apo AII (P < 0.05) and the HDL cholesterol/Apo AII ratio (P < 0.05). Changes in Apo AII and the HDL cholesterol/Apo AII ratio due to dietary oil differed (P < 0.05) in normocholesterolemic and hypercholesterolemic women. The percentage composition of HDL after both dietary periods is shown in Figure 2
.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Saturated fatty acids increase the HDL cholesterol concentration (10
), which has been associated with increased LCAT activity (24
). After consumption of the palmolein diet, the HDL fraction isolated from these subjects appeared enriched in both cholesterol and Apo AII. More specifically, we observed that this effect of increased Apo AII was observed in all women (all had > 20% increase from basal values). Apo AII has been shown to inhibit hepatic lipase (25
), which in turn could contribute to the increase in HDL found in the present study. However, an increase in the Apo AII/HDL cholesterol ratio was found in patients with coronary artery disease (26
), suggesting that in the present study although palmolein increased HDL levels, the decrease in the HDL cholesterol/Apo AII ratio should be interpreted as being associated with an increased atherogenic profile.
In our study, the palmolein diet selectively increased Apo AII, but not Apo AI levels. Therefore, we can postulate that a decrease in LpAI and an increase of LpAI:Apo AII occurred. In transgenic mice, the protective role of LpAI has been confirmed, whereas the increased expression of human Apo AII in such a mouse model promotes rather than delays the development of the fatty streaks (27
).
The mechanisms responsible for the observed effects on Apo AII levels are unknown. A diet high in saturated fatty acids and cholesterol compared with the National Cholesterol Education Program diet results in higher plasma HDL cholesterol in fasting subjects, but the higher Apo AI or Apo AII concentrations were observed only in the LpAI/Apo AII ratio (12
). The lack of a dietary oil effect on Apo AI levels in the present study could be the result of a balance between the decrease in the Apo AI mRNA levels as a result of the decreased intake of monounsaturated fatty acids (28
,29
) and the increase in the saturated fatty acid intake, which increases the level of HDL (10
). Larger sized HDL have an increased cholesterol/Apo AI + Apo AII ratio (30
,31
) and lower catabolic rate. Reductions in dietary total and saturated fat decreased the HDL cholesterol level with more pronounced effects on the large HDL populations (11
). Throughout the study, the molar cholesterol/Apo AI + Apo AII ratio did not change (24.9/1 and 24.3/1 after the high oleic sunflower oil period and the palmolein period, respectively), suggesting a similar HDL average size. However, a detailed study showed that the molar cholesterol/Apo AI/Apo AII ratio was 94.7/2.9/1 and 74.7/2/1 after the high oleic sunflower oil diet and the palmolein diet, respectively, suggesting changes in the HDL average composition.
Differences in the response to diet between normo- and hypercholesterolemic subjects have been suggested (15
,32
–34
). The dietary exchange tended to increase HDL cholesterol to a greater extent in the normocholesterolemics (22.2 vs. 7.5%), suggesting that saturated fatty acids induce a lower Apo AI-mRNA expression in the women with high serum cholesterol levels.
Apo AII increased less in normo- than hypercholesterolemic women (33.3 vs. 47.7%), with no changes in Apo AI. The decrease in the Apo AI/Apo AII ratio tended (P < 0.1) to be higher in hypercholesterolemic subjects (-33.2 vs. -27.4%), suggesting that saturated fatty acids compared with monounsaturated fatty acids decrease the esterification of cholesterol in HDL, and this effect is more marked in women with high serum cholesterol. This is relevant considering the higher cardiovascular risk of hypercholesterolemic subjects. Moreover, the HDL cholesterol/Apo AII ratio decreased more in hypercholesterolemic individuals (-8.7 vs. -29.0%), consistent with previous findings that this ratio is modified in patients with coronary artery disease (26
).
In conclusion, the present study shows that 10% energy substitution of oleic acid by palmitic acid significantly increased HDL cholesterol and Apo AII levels. The increase in Apo AII was greater than that of cholesterol, suggesting an enrichment of HDL in Apo AII and thus a higher CHD risk. This dietary intervention would have more deleterious implications in the hypercholesterolemic population because Apo AII increased and the Apo AI/Apo AII ratio tended to decrease more in these subjects, suggesting that average HDL particles after consumption of the palmolein diet have a lower turnover in the hypercholesterolemic subpopulation with impaired cholesterol reverse transport.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: Apo, apolipoprotein; CHD, coronary heart disease; LCAT, lecithin cholesterol acyl transferase; Lp, lipoproteins.
Manuscript received 11 June 2001. Initial review completed 2 August 2001. Revision accepted 6 October 2001.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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