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Lipids and Atherosclerosis Research Unit, Hospital Universitario Reina Sofía, Córdoba, Spain
2To whom correspondence should be addressed. E-mail: md1lomij{at}uco.es.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • apoE gene polymorphism • diet • LDL size
Apolipoprotein E (apoE)3 plays an important role in lipid metabolism, both promoting efficient uptake of triglyceride-rich lipoproteins (TRL) from the circulation (1,2) and taking part in the cellular cholesterol efflux and reverse cholesterol transport (3). However, such functions are not uniformly effective because apoE is present in the population in 3 main isoforms (apoE2, apoE3, and apoE4). These proteins determine changes in apoE plasma concentrations and differ in their affinity to its specific receptors (4,5).
The apoE4 variant has been associated with increased LDL production from VLDL, increased uptake of postprandial lipoproteins, increased intestinal absorption of cholesterol, decreased bile acid synthesis, and faster LDL clearance from plasma compared with the apoE3 or apoE2 variants (6–8). The apoE2 allele has been consistently associated with lower LDL cholesterol (LDL-C) and apoB levels and higher triacylglycerol, HDL-C and apoA-I concentrations (9–11).
The highest apoB, total cholesterol (TC) and LDL-C levels associated with the apoE4 isoform (12–15) are related to the intake of diets enriched in saturated fat and cholesterol (16,17). These findings led to an examination of the interaction between lipoprotein responsiveness to dietary manipulation and apoE alleles in a number of studies. However, the results have been controversial (18). Although some studies found a pronounced dietary responsiveness for apoE4 carriers, others reported no difference in response across apoE genotypes to changes in dietary fat or cholesterol content (19–21). Thus, the hyperresponse of LDL-C concentrations associated with the E4 allele occurred only when the fat content in the diet varied (22).
Several studies suggested that the presence of small, dense LDL particles is associated with an increased risk of coronary artery disease (CAD) (23). LDL particle size is dependent on both genetic factors and environmental factors such as dietary fat composition. Low-fat, high-carbohydrate diets decreased mean LDL size compared with high saturated fat diets (24,25); the largest and smallest subfractions decreased in concentration, whereas the intermediate-small fraction increased. Monounsaturated fat diets, slightly reduced (26) or did not affect (27) LDL size compared with saturated fat diets. Overall, it is difficult to provide a clinical interpretation to infer benefit or harm from such changes in LDL sizes during these interventions. On the other hand, several authors indicated that the apoE genotype is a major genetic determinant of LDL size although results are contradictory. Although some data show that subjects carrying the apoE2 allele have smaller and denser LDL than subjects carrying the apoE4 allele (28), other studies failed to show this relation (29) or even that subjects carrying apoE4 allele have smaller LDL particle diameter than subjects with the apoE2 allele (15,30). Interestingly, even though both apoE phenotype and diet modify LDL size, studies showing the interaction between these 2 factors are scarce or discrepant. Thus, a higher saturated fat intake was associated with smaller LDL particles in apoE2 subjects, and larger LDL particles in apoE4 subjects (31). However, another study showed that when subjects changed from a high- to a low-fat diet, there was a shift from large, buoyant, cholesterol-rich particles, to smaller, denser LDL particles, with progressively greater reductions in levels of larger LDL from apoE3/2 to apoE3/3 to apoE3/4 (32). Therefore, the aim of this work was to examine whether the apoE genotype interacts with the quantity and quality of dietary fat, modifying LDL size in young healthy subjects.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Diets. The study design included an initial 28-d period during which all subjects consumed a SFA-rich diet, with 15% protein, 47% carbohydrate (CHO) and 38% fat [20% SFA, 12% monounsaturated fatty acid (MUFA) and 6% PUFA]. After this period, volunteers were randomly assigned to 1 of 2 diet sequences. Forty-two subjects consumed a MUFA-rich diet containing 15% protein, 47% CHO and 38% fat (<10% SFA, 6% PUFA, 22% MUFA) for 28 d. This diet was followed for 28 d by consumption of a CHO-rich diet containing 15% protein, 55% carbohydrates and < 30% fat (<10% SFA, 6% PUFA, 12% MUFA). The other 42 subjects consumed the CHO diet before the MUFA diet. The cholesterol content remained constant (<300 mg/d) during the 3 periods. Virgin olive oil comprised 80% of the MUFA diet; it was used for cooking, salad dressing, and as a spread. Carbohydrate intake of the CHO diet was based on the consumption of biscuits, jam, and bread. Butter and palm oil were used during the SFA dietary period.
The composition of the experimental diets was calculated using the USDA (33) food tables and Spanish food composition tables for local foodstuffs (34). All meals were prepared in the hospital kitchen and were supervised by a dietitian. Lunch and dinner were eaten in the hospital dining room, whereas breakfast and an afternoon snack were eaten in the medical school cafeteria. Menus (n = 14) were prepared with regular solid foods and rotated during the experimental period. Duplicate samples from each menu were collected, homogenized, and stored at –70°C. Protein, fat, and carbohydrate contents of the diet were analyzed by standard methods (35). Dietary compliance was verified by analyzing the fatty acids in LDL-C esters at the end of each dietary period (36). The study took place from January to March to minimize seasonal effects and academic stress.
Lipid analysis, biochemical determinations, and LDL size.
Venous blood samples were collected into EDTA-containing (1 g/L) tubes from all subjects after a 12-h overnight fast at the beginning of the study and at the end of each dietary period. Plasma was obtained by low-speed centrifugation (1500 x g) for 15 min at 4°C within 1 h of venipuncture. To reduce interassay variation, plasma was stored at –80°C and analyzed at the end of the study. Plasma TC and triacylglycerol levels were determined by enzymatic techniques (37,38). HDL-C was determined after precipitation with phosphotungstic acid (39). Apo A-I and apo B were determined by immunoturbidimetry (40). LDL-C concentration was calculated using the Friedewald formula (41). The predominant LDL peak particle diameter (LDL size) was measured from serum samples with polyacrylamide gradient gel electrophoresis as described (42). We identified 2 subclass LDL-phenotypes using the criteria described previously (43): the classical category, phenotype A, is >25.5 nm, and phenotype B is 
25.5 nm.
DNA amplification and genotyping of apoE. Amplification of a region of 266 bp of the apoE gen was done by PCR with 250 ng of genomic DNA and 0.2 µmol of each oligonucleotide primer (E1, 5'-GAACAACTGACCCCGGTGGCGGAG-3', and E2, 5'-TCGCGGGCCCCGGCCTGGTACACTGCCA-3') and 10% dimethyl sulfoxide in 50 µL. DNA was denatured at 95°C for 5 min followed by 30 cycles of denaturation at 95°C for 1 min, annealing at 63°C for 1.5 min, and extension at 72°C for 2 min. The PCR product (20 µL) was digested with 10 U of restriction enzyme CfoI (BRL) in a total volume of 35 µL. Digested DNA was separated by electrophoresis on an 8% nondenaturing polyacrylamide gel at 150 V for 2 h. Bands were visualized by silver staining.
Statistical analysis. ANOVA for repeated measures was used to test for the effects of the apoE gene polymorphism on plasma TC, LDL-C, HDL-C, triacylglycerol, apo A-I, and apo B concentration and LDL size in each dietary stage. Triacylglycerols levels were log transformed before statistical analyses. When statistical significance was found, Tukey’s post-hoc comparison test was used to identify group differences. Independent sample t-test was used to detect if women had greater LDL-size and higher HDL-C and apoA-I plasma concentration than men after each dietary period.
The 
2 test was used to determine whether the replacement of high-fat diets (SFA or MUFA) by a low-fat, high-CHO increased the number of subjects with LDL-phenotype B. Differences were considered significant at P < 0.05. Statistical analyses were conducted using the SPSS statistical software, version 8.0 (SPSS).
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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A diet high in saturated fat contributes to the development of CAD; thus, dietary intervention is recommended to lower plasma lipid levels. However, it is not clear whether saturated fat should be replaced by carbohydrates or monounsaturated fat. In accordance with our results, previous studies indicated that both MUFA and CHO diets reduce TC and LDL-C (44,45). However, when subjects consumed a MUFA diet the levels of HDL-C and apoA-I were higher compared with those consuming a CHO diet. In addition, we observed that low-fat, high-carbohydrate diets compared with high saturated fat decreased the mean LDL size (24,25,31,32). Furthermore, our data confirm the results obtained in a recent study in which no differences in LDL size were observed between MUFA and SFA diets (27). But more importantly, our study shows that a Mediterranean diet enriched in MUFA increases LDL size in comparison with a low-fat, high-carbohydrate diet. Studies employing analysis of LDL subclasses demonstrated heterogeneity of the LDL response to low-fat, high-carbohydrate diets in healthy subjects (46). In individuals with a genetically influenced atherogenic lipoprotein phenotype, characterized by a predominance of small dense LDL (phenotype B), lowering of plasma LDL cholesterol levels by low-fat diets represents a reduction in the numbers of circulating small LDL particles. In contrast, in the majority of healthy individuals with larger LDL (phenotype A), a significant proportion of the low-fat diet-induced reduction in plasma LDL cholesterol is due to depletion of the cholesterol content of LDL particles and the shift from larger to smaller LDL particle diameters. Moreover, with a progressive reduction of dietary fat and isoenergetic substitution of carbohydrate, an increasing number of subjects with phenotype A convert to the phenotype B, as noted here.
One of the most intriguing aspects of the response of plasma cholesterol to diet is how it varies among individuals. The influence of the genetic loci of the principal apolipoproteins such as the AI-CIII-AIV complex and the apoE gene has been studied (22,47,48). In agreement with previous studies (9,10), we observed that the presence of the apoE4 allele is associated with a proatherogenic lipoprotein profile, with increased apoB, TC, and LDL-C plasma concentrations. The effect of the apoE genotypes on plasma lipids is modified by environmental factors such as dietary intake (12,49). Thus, the hyperresponse of LDL-C concentrations associated with the E4 allele occurred only when the fat content in the diet varied (23). We observed that replacement of a CHO diet by a MUFA diet was associated with a significant decrease in LDL-C in apoE 3/4 subjects, whereas the opposite or no effect was observed for apoE 3/2 and apoE 3/3 subjects, respectively.
The relation between apoE genotype and LDL size provided contrasting results (15,26,28–31,50). In accordance with previous studies, we observed that apoE2 subjects had smaller LDL particles than the other groups (29,31,50) and changes in LDL size were inversely correlated with triacylglycerol levels (28). The mechanism by which apoE isoforms might affect LDL particle size is not completely clear. Barballo et al. (50) speculate that this genetic response probably involves the effect of apoE2 on receptor-mediated VLDL clearance. Thus, the decreased uptake of VLDL and VLDL remnants by the B/E receptor in apoE2 subjects leads to higher levels of TRL with an increased conversion into smaller and denser LDL particles. However, other studies reported that apoE2 subjects have similar or even larger LDL particles compared with apoE3 and apoE4 individuals (15,30,31). Environmental factors, such as diet or geographical differences, could explain the variability observed in these studies. In agreement with this hypothesis, some studies examined the effect of apoE gene-diet interaction on LDL-size. Thus, Campos et al. (31) divided free-living Costa Ricans according to their intake of saturated fat and observed that higher saturated fat intake was associated with smaller LDL particles in apoE2 subjects, and larger LDL particles in apoE4 subjects. However the gene-diet interaction was not significant for LDL particle size. This study was conducted in a population under normal daily conditions without dietary intervention. In our study, subjects were randomly assigned to a dietary intervention study, which means that the results obtained are more reliable. Thus, the replacement of a CHO diet by a MUFA diet increases LDL-size in apoE 3/3, whereas it decreases it in apoE 4/3 subjects. We also observed that LDL-size was larger in apoE 4/3 subjects than in apoE 3/3 and apoE 3/2 subjects after the SFA, CHO, and MUFA diets. However, Dreon et al. (32) found that reduction in dietary fat resulted in a shift from large, buoyant, cholesterol-rich particles to smaller, denser, LDL particles, with progressively greater reductions in levels of larger LDL from apoE 3/2 to apoE 3/3 to apoE 3/4. Their results apply only to reduction in total fat intake, and it is possible that apoE isoforms operate differently in influencing the response to other dietary manipulation, such as substitution of monounsaturated fat or carbohydrates for saturated fat intake.
Studies in vitro demonstrated that oleic acid is a potent stimulator of TRL secretion (51), and test-meal studies found that meals high in oleic acid–rich oils caused a more pronounced, sharper postprandial rise in plasma TRL than SFA-rich meals (52). The apoE4 variant was associated with increased uptake of postprandial lipoproteins compared with the apoE3 or apoE2 variants (6). Therefore, apoE4 subjects would have lower levels of TRL with a decreased conversion into smaller and denser LDL particles (24). A MUFA diet, high in oleic acid from virgin olive oil, could regulate the increased uptake of TRL in apoE4 subjects. This would explain the decrease in LDL particle size observed in our study when apoE4 subjects changed from a CHO diet to a MUFA diet. We observed this effect only in apoE4 subjects likely because carriers of the apoE4 allele have a greater lipid response to dietary changes than individuals not possessing the apoE4 allele (22). Although increased intake of carbohydrates may decrease LDL size (24,25), it is not known whether reduced dietary fat intake contributes to these lipoprotein changes to a lesser extent than the MUFA diet, as we observed. New studies are warranted, therefore, to confirm our results. It is important to note that one of the limitations to genetic association studies is the difficulty in corroborating findings observed in populations with different characteristics. We must be cautious therefore when extrapolating the results to a more general population.
In conclusion, our data indicate that each subject has to be examined and guided individually when dietary recommendations are made. No diet can be recommended unequivocally without knowing more about those being targeted. Even though a MUFA-rich diet increases LDL size compared with a CHO-rich diet, this effect is dependent on apoE genotypes. Thus, the replacement of a CHO diet by a MUFA diet increases LDL-size in apoE 3/3, whereas it decreases it in apoE 4/3 subjects.
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FOOTNOTES |
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3 Abbreviations used: apo, apolipoprotein; CAD, coronary artery disease, CHO, carbohydrate; HDL-C, HDL cholesterol; LDL-C, LDL cholesterol; MUFA, monounsaturated fatty acid; TC, total cholesterol; TRL, triacylglycerol rich lipoproteins.
Manuscript received 5 May 2004. Initial review completed 8 June 2004. Revision accepted 14 July 2004.
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LITERATURE CITED |
|---|
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Beisiegel, U., Weber, W., Ihrke, G., Herz, J. & Stanley, K. K. (1989) The LDL-receptor-related protein, LRP, is an apolipoprotein E-binding protein. Nature (Lond.) 14:162-164.
2. Weisgraber, K. H. (1994) Apolipoprotein E: structure-function relationships. Adv. Protein Chem. 45:249-302.[Medline]
3. Miettinen, T. A., Gylling, H., Vanhanen, H. & Ollus, A. (1992) Cholesterol absorption, elimination, and synthesis related to LDL kinetics during fat intake in men with different apoprotein E phenotypes. Arterioscler. Thromb. 12:1044-1052.
4. Mahley, R. W. (1988) Apolipoprotein E: cholesterol transport protein with expanding role in cell biology 240:622-630 Science Washington, DC.
5. Mahley, R. W. & Huang, Y. (1999) Apolipoprotein E: from atherosclerosis to Alzheimer’s disease and beyond. Curr. Opin. Lipidol. 10:207-217.[Medline]
6. Gylling, H., Kontula, K. & Miettinen, T. A. (1995) Cholesterol absorption and metabolism and LDL kinetics in healthy men with different apoprotein E phenotypes and apoprotein B XbaI and LDL receptor PvuII genotypes. Arterioscler. Thromb. Vasc. Biol. 15:208-213.
7. Weintraub, M. S., Eisenberg, S. & Breslow, J. L. (1987) Dietary fat clearance in normal subjects is regulated by genetic variation in apolipoprotein E. J. Clin. Investig. 80:1571-1577.
8. Nikkilä, M., Solakivi, T., Lehtimäki, T., Koivula, T., Laippala, P. & Astrom, B. (1994) Postprandial plasma lipoprotein changes in relation to apolipoprotein E phenotypes and low density lipoprotein size in men with and without coronary artery disease. Atherosclerosis 106:149-157.[Medline]
9. Dallongeville, J., Lussier-Cacan, S. & Davignon, J. (1992) Modulation of plasma triglyceride levels by apoE phenotype: a meta-analysis. J. Lipid Res. 33:447-454.[Abstract]
10. Wilson, P.W.F., Myers, R. H., Larson, M. G., Ordovas, J. M., Wolf, P. A. & Schaefer, E. J. (1994) Apolipoprotein E alleles, dyslipidemia, and coronary heart disease: the Framingham offspring study. J. Am. Med. Assoc. 272:1666-1671.
11. Kataoka, S., Robbins, D. C., Cowan, L. D., Go, O., Yeh, J. L., Devereus, R. B., Fabsitz, R. R., Lee, E. T., Welty, T. K. & Howard, B. V. (1996) Apolipoprotein E polymorphism in American Indians and its relation to plasma lipoproteins and diabetes: the Strong Heart Study. Arterioscler. Thromb. Vasc. Biol. 16:918-925.
12. Davignon, J., Gregg, R. E. & Sing, C. F. (1988) Apolipoprotein E polymorphism and atherosclerosis. Arteriosclerosis 8:1-21.
13. Wilson, P. W., Schaefer, E. J. & Larson, M. G. (1996) Apolipoprotein E alleles and risk of coronary disease. A meta-analysis. Arterioscler. Thromb. Vasc. Biol. 16:1250-1255.
14. Utermann, G., Pruin, N. & Steinmetz, A. (1979) Polymorphism of apolipoprotein E. Effect of a single polymorphic gene locus on plasma lipid levels in men. Clin. Genet. 15:63-72.[Medline]
15. Schaefer, E. J., Lamon-Fava, S., Johnson, S., Ordovas, J. M., Schaefer, M. M., Castelli, W. P. & Wilson, P. W. (1994) Effects of gender and menopausal status on the association of apolipoprotein E phenotype with plasma lipoprotein levels. Arterioscler. Thromb. 14:1105-1113.
16. Ehnholm, C., Lukka, M., Kuusi, T., Nikkila, E. & Utermann, G. (1986) Apolipoprotein E polymorphism in the Finnish population: gene frequencies and relation to lipoprotein concentrations. J. Lipid Res. 27:227-235.[Abstract]
17. Utermann, G. (1987) Apolipoprotein E polymorphism in health and disease. Am. Heart J. 113:433-440.[Medline]
18. Rubin, J. & Berglund, L. (2002) Apolipoprotein E and diets: a case of gene-nutrient interaction?. Curr. Opin. Lipidol. 13:25-32.[Medline]
19. Talmud, P. J. & Waterworth, D. M. (2000) In-vivo and in-vitro nutrient-gene interactions. Curr. Opin. Lipidol. 11:31-36.[Medline]
20. Ordovas, J. M. & Schaefer, E. J. (1999) Genes, variation of cholesterol and fat intake and serum lipids. Curr. Opin. Lipidol. 10:15-22.[Medline]
21. Weggemans, R. M., Zock, P. L., Ordovas, J. M., Pedro-Botet, J. & Katan, M. B. (2001) Apolipoprotein E genotype and the response of serum cholesterol to dietary fat, cholesterol and cafestol. Atherosclerosis 154:547-555.[Medline]
22. Lopez-Miranda, J., Ordovas, J. M., Mata, P., Lichtenstein, A. H., Clevidence, B. & Judd, J. T. (1994) Effect of apolipoprotein E phenotype on diet induced plasma low density lipoprotein cholesterol lowering. J. Lipid Res. 35:1965-1975.[Abstract]
23. Campos, H., Genest, J. J., Jr, Blijlevens, E., McNamara, J. R., Jenner, J. L., Ordovas, J. M., Wilson, P. W. & Schaefer, E. J. (1992) Low density lipoprotein particle size and coronary artery disease. Arterioscler. Thromb. 12:187-195.
24. Dreon, D. M., Fernstrom, H. A., Williams, P. T. & Krauss, R. M. (1999) A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins. Am. J. Clin. Nutr. 69:411-418.
25. Krauss, R. M. & Dreon, D. M. (1995) Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men. Am. J. Clin. Nutr. 629:478-487.
26. Kratz, M., Gulbahce, E., von Eckardstein, A., Cullen, P., Cignarella, A., Assmann, G. & Wahrburg, U. (2002) Dietary mono- and polyunsaturated fatty acids similarly affect LDL size in healthy men and women. J. Nutr. 132:715-718.
27. Rivellese, A. A., Maffettone, A., Vessby, B., Uusitupa, M., Hermansen, K., Berglund, L., Louheranta, A., Meyer, B. J. & Riccardi, G. (2003) Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects. Atherosclerosis 167:149-158.[Medline]
28. Dart, A. M. & Cooper, B. (1999) Independent effects of Apo E phenotype and plasma triglyceride on lipoprotein particle sizes in the fasting and postprandial states. Arterioscler. Thromb. Vasc. Biol. 19:2465-2473.
29. Zhao, S. P., Verhoeven, M. H., Vink, J., Hollaar, L., van der Laarse, A., de Knijff, P. & van’t Hooft, F. M. (1993) Relationship between apolipoprotein E and low density lipoprotein particle size. Atherosclerosis 102:147-154.[Medline]
30. Haffner, S. M., Stern, M. P., Miettinen, H., Robbins, D. & Howard, B. V. (1996) Apolipoprotein E polymorphism and LDL size in a biethnic population. Arterioscler. Thromb. Vasc. Biol. 16:1184-1188.
31. Campos, H., D’Agostino, M. & Ordovas, J. M. (2001) Gene-diet interactions and plasma lipoproteins: role of apolipoprotein E and habitual saturated fat intake. Genet. Epidemiol. 20:117-128.[Medline]
32. Dreon, D. M., Fernstrom, H. A., Miller, B. & Krauss, R. M. (1995) Apolipoprotein E isoform phenotype and LDL subclass response to a reduce fat diet. Arterioscler. Thromb. Vasc. Biol. 15:105-111.
33. Human Nutrition Information Service (1987) Department of Agriculture Composition of Foods, Agriculture Handbook no. 8 1987 U.S. Government Printing Office Washington, DC.
34. Varela, G. (1980) Food Composition Tables (Tablas de Composición de Alimentos) 1980 Instituto de Nutrición, CSIC Madrid, Spain.
35. Association of Official Analytical Chemists (1990) Official Methods of Analysis 15th ed. 1990 Association of Official Analytical Chemists Arlington, VA.
36. Ruiz-Gutiérrez, V., Prada, J. L. & Pérez-Jiménez, F. (1993) Determination of fatty acid and triacylglycerol composition of human very-low-density lipoproteins. J. Chromatogr. 622:117-134.[Medline]
37. Allain, C. C., Poon, L. S., Chang, C. S., Richmond, W. & Fu, P. C. (1974) Enzymatic determination of total serum cholesterol. Clin. Chem. 20:470-475.[Abstract]
38. Bucolo, G. & David, H. (1973) Quantitative determination of serum triglycerides by use of enzymes. Clin. Chem. 19:476-482.[Abstract]
39. Assmann, G., Schierwer, H., Schmitz, G. & Hägele, E. (1983) Quantification of high density lipoprotein cholesterol by precipitation with phosphotungstic acid-MgCl2. Clin. Chem. 29:2026-2030.
40. Riepponem, P., Marniemi, J. & Rautaoja, T. (1987) Immunoturbidimetric determination of apolipoproteins A-I and B in serum. Scand. J. Clin. Lab. Investig. 47:739-744.[Medline]
41. Friedewald, W. T., Levy, R. I. & Fredrickson, D. S. (1972) Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of a preparative ultracentrifuge. Clin. Chem. 18:499-502.[Abstract]
42. Krauss, R. M. & Burke, D. J. (1982) Identification of multiple subclasses of plasma low density lipoproteins in normal humans. J. Lipid Res. 23:97-104.[Abstract]
43. Austin, M. A. & Krauss, R. M. (1986) Genetic control of low-density lipoprotein subclasses. Lancet 2:592-595.[Medline]
44. Mensink, R. P. & Katan, M. B. (1991) Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler. Thromb. 12:911-919.
45. Hegsted, D. M., Ausman, L. M., Johnson, J. A. & Dallal, G. E. (1993) Dietary fat and serum lipids: an evaluation of the experimental data. Am. J. Clin. Nutr. 57:875-883.
46. Krauss, R. M. (2001) Atherogenic lipoprotein phenotype and diet-gene interaction. J. Nutr. 131:340-343.
47. Lopez-Miranda, J., Jansen, S., Ordovas, J. M., Salas, J., Marin, C., Castro, P., Ostos, M. A., Cruz, G., Lopez-Segura, F., Blanco, A., Jimenez-Pereperez, J. & Perez-Jimenez, F. (1997) Influence of the SstI polymorphism at the apolipoprotein C-III gene locus on the plasma low-density-lipoprotein-cholesterol response to dietary monounsaturated fat. Am. J. Clin. Nutr. 66:97-103.
48. Lopez-Miranda, J., Ordovas, J. M., Espino, A., Marin, C., Salas, J., Lopez Segura, F. & Perez-Jimenez, F. (1994) Human apolipoprotein A-I gene promoter mutation predicts plasma low density lipoprotein cholesterol response to dietary fat in young males. Lancet 343:1246-1249.[Medline]
49. Luc, G., Bard, J. M., Arvellier, D., Evans, A., Cambou, J. P., Bingham, A., Amouyel, P., Schaffer, P., Ruidavets, J. B., Cambien, F., Fruckhart, J. C. & Lucimetiere, P. (1994) Impact of apolipoprotein E polymorphism on lipoproteins and risk of myocardial infarction: the ECTIM study. Arterioscler. Thromb. 14:1412-1419.
50. Barbagallo, C. M., Polizzi, F., Severino, M., Rizzo, M., Vivona, N., Onorato, F., Caldarella, R., Cefalu, A. B., Noto, D., Notarbartolo, A. & Averna, M. R. (2001) ApoE polymorphism in a small Mediterranean island: relationships with plasma lipids, lipoproteins and LDL particle size. Eur. J. Epidemiol. 17:707-713.[Medline]
51. Black, I. L., Roche, H. M., Tully, A. M. & Gibney, M. J. (2002) Acute-on-chronic effects of fatty acids on intestinal triacylglycerol-rich lipoprotein metabolism. Br. J. Nutr. 88:661-669.[Medline]
52. Sanders, T. A., de Grassi, T., Miller, G. J. & Morrissey, J. H. (2000) Influence of fatty acid chain length and cis/trans isomerization on postprandial lipemia and factor VII in healthy subjects (postprandial lipids and factor VII). Atherosclerosis 149:413-420.[Medline]
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