Nos résultats apportent de nouvelles perspectives par rapport à la littérature déjà publiée concernant les effets de gras alimentaires sur la CEC stimulée par les HDL.
D'abord, certaines limites doivent être considérées. Entre autres, il est difficile de déterminer à quel point la mesure de la CEC ex vivo, telle que dans la présente étude, témoigne avec justesse des processus in vivo. Dans le même contexte, il n'est pas connu à quel point le cholestérol récupéré par les particules HDL à l'étape de l'efflux de cholestérol pourra ensuite être excrété au foie. Dans ce sens, la CEC n'est qu'une courte portion de l'ensemble du transport inverse du cholestérol et la manière dont les gras alimentaires influencent les étapes subséquentes n'est pas connue. Finalement, notre intervention à court terme montre que les gras alimentaires peuvent induire des différences statistiquement significatives de CEC. Cependant, il n'est pas possible de déterminer si ces différences seront cliniquement significatives par rapport au risque de MCV à moyen ou long terme.
Il semble que les changements induits par l'alimentation sur les sous-classes (mesurées par GGE une dimension) ou la composition lipidique (mesurée par chromatographie en phase gazeuse) des HDL n'expliquent pas les changements d'efflux de cholestérol. Ainsi, nos résultats ne montrent pas de liens clairs entre les caractéristiques physiques mesurés par ces méthodes et les changements de CEC après une intervention nutritionnelle. Ces observations n'excluent pas que des techniques différentes (évaluation de la charge par GGE à deux dimensions) ou d'autres investigations (composition en protéines des HDL) pourraient expliquer les différences d'efflux de cholestérol entre les diètes.
Ensuite, nous avons observé des effets différents de diètes riches en AGS provenant du beurre et du fromage sur la CEC, malgré une teneur similaire en AGS. Ainsi, un effet de la matrice alimentaire du fromage semble interférer avec
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l'impact des AGS laitiers, confirmant notre première hypothèse de recherche. D'autres investigations devront confirmer cette observation, puisque notre étude est la première à évaluer l'influence de la source alimentaire des gras sur la CEC. Dans le même ordre d'idées, il conviendra de vérifier quel(s) facteur(s) nutritionnel(s) provoquent l'effet matrice.
Finalement, nous avons comparé les diètes riches en AGS à d'autres gras (MONO et POLY). La diète BEURRE a augmenté la CEC chez les hommes seulement et cette augmentation fut associée à l'augmentation concomitante des concentrations de LDL-C. Cette dernière observation suppose peut-être un mécanisme compensatoire de l'effet hypercholestérolémiant des AGS du beurre. Bien que cette hypothèse soit cohérente avec de récentes études épidémiologiques (9, 93), d'autres auteurs devront valider notre observation. D'autre part, Les diètes MONO et POLY ont augmenté la CEC, mais chez les femmes seulement; la cause exacte de ce dimorphisme sexuel est inconnue. Notons que le fromage n'a pas stimulé la CEC chez les hommes ni chez les femmes.
En somme, l'effet de la matrice alimentaire, l'hypothèse de la compensation de la CEC en réponse aux effets hypercholestérolémiants des AGS du beurre et le dimorphisme sexuel quant à l'impact des AGS et des gras insaturés sont des résultats qui apportent certaines réponses, mais beaucoup de questions. L'évaluation de nouvelles mesures de fonctionnalité (par exemple, la capacité antioxydante), la caractérisation du protéome (composition protéique des HDL) ou l'évaluation de la charge des HDL sont des informations supplémentaires qui permettront d'approfondir nos observations sur la CEC induite par une intervention nutritionnelle et de clarifier l'impact des gras alimentaires sur les HDL. De nouvelles études d'intervention contrôlée devront aussi évaluer la causalité de la CEC dans le développement des MCV.
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Bibliographie
1. Moore KJ, Sheedy FJ, Fisher EA. Macrophages in atherosclerosis: a dynamic balance. Nat Rev Immunol 2013;13:709-21.
2. Herrington W, Lacey B, Sherliker P, Armitage J, Lewington S. Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of
Atherothrombotic Disease. Circ Res 2016;118:535-46.
3. Collaborators GRF. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 2016;388:1659-724.
4.Canada Adlspd. Système canadien de surveillance des maladies chroniques fournis par les provinces et les territoires. 2015.
5. Anderson TJ, Grégoire J, Pearson GJ, Barry AR, Couture P, Dawes M, Francis GA, Genest J, Grover S, Gupta M, et al. 2016 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult. Can J Cardiol 2016;32:1263-82.
6. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, Franco OH, Butterworth AS, Forouhi NG, Thompson SG, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med 2014;160:398-406.
7. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010;91:535-46.
8. de Oliveira Otto MC, Mozaffarian D, Kromhout D, Bertoni AG, Sibley CT, Jacobs DR, Nettleton JA. Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis. Am J Clin Nutr 2012;96:397-404.
9. Praagman J, Beulens JW, Alssema M, Zock PL, Wanders AJ, Sluijs I, van der Schouw YT. The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the
European Prospective Investigation into Cancer and Nutrition-Netherlands cohort. Am J Clin Nutr 2016;103:356-65.
10. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77:1146-55.
11. Gordon DJ, Probstfield JL, Garrison RJ, Neaton JD, Castelli WP, Knoke JD, Jacobs DR, Bangdiwala S, Tyroler HA. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation 1989;79:8- 15.
12. Toth PP, Barter PJ, Rosenson RS, Boden WE, Chapman MJ, Cuchel M, D'Agostino RB, Davidson MH, Davidson WS, Heinecke JW, et al. High-density lipoproteins: a consensus statement from the National Lipid Association. J Clin Lipidol 2013;7:484-525.
13. Voight BF, Peloso GM, Orho-Melander M, Frikke-Schmidt R, Barbalic M, Jensen MK, Hindy G, Hólm H, Ding EL, Johnson T, et al. Plasma HDL cholesterol
81
and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012;380:572-80.
14. Arsenault BJ, Després JP. HDL cholesterol is not HDL--don't judge the book by its cover. Nat Rev Cardiol 2012;9:557-8.
15. Rohatgi A. High-Density Lipoprotein Function Measurement in Human Studies: Focus on Cholesterol Efflux Capacity. Prog Cardiovasc Dis 2015;58:32- 40.
16. Moore KJ, Freeman MW. Scavenger receptors in atherosclerosis: beyond lipid uptake. Arterioscler Thromb Vasc Biol 2006;26:1702-11.
17. Moore KJ, Tabas I. Macrophages in the pathogenesis of atherosclerosis. Cell 2011;145:341-55.
18. Maxfield FR, Tabas I. Role of cholesterol and lipid organization in disease. Nature 2005;438:612-21.
19. Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res 2014;114:1852-66.
20. DAWBER TR, MOORE FE, MANN GV. Coronary heart disease in the Framingham study. Am J Public Health Nations Health 1957;47:4-24.
21. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ 2004;328:1519.
22. Pirie K, Peto R, Reeves GK, Green J, Beral V, Collaborators MWS. The 21st century hazards of smoking and benefits of stopping: a prospective study of one million women in the UK. Lancet 2013;381:133-41.
23. Baigent C, Blackwell L, Emberson J, Holland LE, Reith C, Bhala N, Peto R, Barnes EH, Keech A, Simes J, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26
randomised trials. Lancet 2010;376:1670-81.
24. Mihaylova B, Emberson J, Blackwell L, Keech A, Simes J, Barnes EH, Voysey M, Gray A, Collins R, Baigent C, et al. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta- analysis of individual data from 27 randomised trials. Lancet 2012;380:581-90. 25. Fulcher J, O'Connell R, Voysey M, Emberson J, Blackwell L, Mihaylova B, Simes J, Collins R, Kirby A, Colhoun H, et al. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet 2015;385:1397-405.
26. Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC, Investigators TtNT. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N Engl J Med 2007;357:1301-10. 27. Wolfram RM, Brewer HB, Xue Z, Satler LF, Pichard AD, Kent KM, Waksman R. Impact of low high-density lipoproteins on in-hospital events and one-year
clinical outcomes in patients with non-ST-elevation myocardial infarction acute coronary syndrome treated with drug-eluting stent implantation. Am J Cardiol 2006;98:711-7.
28. Rosenson RS, Brewer HB, Chapman MJ, Fazio S, Hussain MM, Kontush A, Krauss RM, Otvos JD, Remaley AT, Schaefer EJ. HDL measures, particle
heterogeneity, proposed nomenclature, and relation to atherosclerotic cardiovascular events. Clin Chem 2011;57:392-410.
82
29. Superko HR, Pendyala L, Williams PT, Momary KM, King SB, Garrett BC. High-density lipoprotein subclasses and their relationship to cardiovascular disease. J Clin Lipidol 2012;6:496-523.
30. Després JP, Lemieux I, Dagenais GR, Cantin B, Lamarche B. HDL-
cholesterol as a marker of coronary heart disease risk: the Québec cardiovascular study. Atherosclerosis 2000;153:263-72.
31. O'Meara NM, Lewis GF, Cabana VG, Iverius PH, Getz GS, Polonsky KS. Role of basal triglyceride and high density lipoprotein in determination of
postprandial lipid and lipoprotein responses. J Clin Endocrinol Metab 1992;75:465- 71.
32. Movva R, Rader DJ. Laboratory assessment of HDL heterogeneity and function. Clin Chem 2008;54:788-800.
33. Lewis GF, Rader DJ. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ Res 2005;96:1221-32.
34. Schwartz GG, Olsson AG, Abt M, Ballantyne CM, Barter PJ, Brumm J, Chaitman BR, Holme IM, Kallend D, Leiter LA, et al. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 2012;367:2089-99. 35. Kaur N, Pandey A, Negi H, Shafiq N, Reddy S, Kaur H, Chadha N, Malhotra S. Effect of HDL-raising drugs on cardiovascular outcomes: a systematic review and meta-regression. PLoS One 2014;9:e94585.
36. Blanche PJ, Gong EL, Forte TM, Nichols AV. Characterization of human high-density lipoproteins by gradient gel electrophoresis. Biochim Biophys Acta 1981;665:408-19.
37. Pérusse M, Pascot A, Després JP, Couillard C, Lamarche B. A new method for HDL particle sizing by polyacrylamide gradient gel electrophoresis using whole plasma. J Lipid Res 2001;42:1331-4.
38. Siri-Tarino PW. Effects of diet on high-density lipoprotein cholesterol. Curr Atheroscler Rep 2011;13:453-60.
39. Williams PT, Dreon DM, Krauss RM. Effects of dietary fat on high-density- lipoprotein subclasses are influenced by both apolipoprotein E isoforms and low- density-lipoprotein subclass patterns. Am J Clin Nutr 1995;61:1234-40.
40. Berglund L, Oliver EH, Fontanez N, Holleran S, Matthews K, Roheim PS, Ginsberg HN, Ramakrishnan R, Lefevre M. HDL-subpopulation patterns in
response to reductions in dietary total and saturated fat intakes in healthy subjects. Am J Clin Nutr 1999;70:992-1000.
41. Rye KA, Barter PJ. Cardioprotective functions of HDLs. J Lipid Res 2014;55:168-79.
42. Zannis VI, Chroni A, Krieger M. Role of apoA-I, ABCA1, LCAT, and SR-BI in the biogenesis of HDL. J Mol Med (Berl) 2006;84:276-94.
43. Heinecke JW. Small HDL promotes cholesterol efflux by the ABCA1 pathway in macrophages: implications for therapies targeted to HDL. Circ Res 2015;116:1101-3.
44. Du XM, Kim MJ, Hou L, Le Goff W, Chapman MJ, Van Eck M, Curtiss LK, Burnett JR, Cartland SP, Quinn CM, et al. HDL particle size is a critical determinant of ABCA1-mediated macrophage cellular cholesterol export. Circ Res
83
45. März W, Ritsch A. Cholesterol Efflux Capacity: Choke Point of Reverse Cholesterol Traffic? J Am Coll Cardiol 2016;67:2488-91.
46. Rothblat GH, de la Llera-Moya M, Atger V, Kellner-Weibel G, Williams DL, Phillips MC. Cell cholesterol efflux: integration of old and new observations provides new insights. J Lipid Res 1999;40:781-96.
47. Cano N, Barnoud D, Schneider SM, Vasson M-P, Hasselmann M, Leverve X. Traité de nutrition artificielle de l'adulte. 3 ed. Paris: Springer-Verlag; 2007. 1191 p.
48. Rust S, Rosier M, Funke H, Real J, Amoura Z, Piette JC, Deleuze JF, Brewer HB, Duverger N, Denèfle P, et al. Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1. Nat Genet 1999;22:352- 5.
49. Young SG, Fielding CJ. The ABCs of cholesterol efflux. Nat Genet 1999;22:316-8.
50. Yvan-Charvet L, Ranalletta M, Wang N, Han S, Terasaka N, Li R, Welch C, Tall AR. Combined deficiency of ABCA1 and ABCG1 promotes foam cell
accumulation and accelerates atherosclerosis in mice. J Clin Invest 2007;117:3900-8.
51. Adorni MP, Zimetti F, Billheimer JT, Wang N, Rader DJ, Phillips MC, Rothblat GH. The roles of different pathways in the release of cholesterol from macrophages. J Lipid Res 2007;48:2453-62.
52. Wang N, Silver DL, Costet P, Tall AR. Specific binding of ApoA-I, enhanced cholesterol efflux, and altered plasma membrane morphology in cells expressing ABC1. J Biol Chem 2000;275:33053-8.
53. Oram JF, Lawn RM, Garvin MR, Wade DP. ABCA1 is the cAMP-inducible apolipoprotein receptor that mediates cholesterol secretion from macrophages. J Biol Chem 2000;275:34508-11.
54. Khera AV, Cuchel M, de la Llera-Moya M, Rodrigues A, Burke MF, Jafri K, French BC, Phillips JA, Mucksavage ML, Wilensky RL, et al. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N Engl J Med 2011;364:127-35.
55. Rohatgi A, Khera A, Berry JD, Givens EG, Ayers CR, Wedin KE, Neeland IJ, Yuhanna IS, Rader DR, de Lemos JA, et al. HDL cholesterol efflux capacity and incident cardiovascular events. N Engl J Med 2014;371:2383-93.
56. Ritsch A, Scharnagl H, März W. HDL cholesterol efflux capacity and cardiovascular events. N Engl J Med 2015;372:1870-1.
57. Kennedy MA, Barrera GC, Nakamura K, Baldán A, Tarr P, Fishbein MC, Frank J, Francone OL, Edwards PA. ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation. Cell Metab 2005;1:121-31.
58. Wang N, Lan D, Chen W, Matsuura F, Tall AR. ATP-binding cassette transporters G1 and G4 mediate cellular cholesterol efflux to high-density lipoproteins. Proc Natl Acad Sci U S A 2004;101:9774-9.
59. Wang N, Ranalletta M, Matsuura F, Peng F, Tall AR. LXR-induced redistribution of ABCG1 to plasma membrane in macrophages enhances cholesterol mass efflux to HDL. Arterioscler Thromb Vasc Biol 2006;26:1310-6.
84
60. Vrins C, Vink E, Vandenberghe KE, Frijters R, Seppen J, Groen AK. The sterol transporting heterodimer ABCG5/ABCG8 requires bile salts to mediate cholesterol efflux. FEBS Lett 2007;581:4616-20.
61. Yu XH, Qian K, Jiang N, Zheng XL, Cayabyab FS, Tang CK.
ABCG5/ABCG8 in cholesterol excretion and atherosclerosis. Clin Chim Acta 2014;428:82-8.
62. Thuahnai ST, Lund-Katz S, Dhanasekaran P, de la Llera-Moya M, Connelly MA, Williams DL, Rothblat GH, Phillips MC. Scavenger receptor class B type I- mediated cholesteryl ester-selective uptake and efflux of unesterified cholesterol. Influence of high density lipoprotein size and structure. J Biol Chem
2004;279:12448-55.
63. Yancey PG, de la Llera-Moya M, Swarnakar S, Monzo P, Klein SM, Connelly MA, Johnson WJ, Williams DL, Rothblat GH. High density lipoprotein phospholipid composition is a major determinant of the bi-directional flux and net movement of cellular free cholesterol mediated by scavenger receptor BI. J Biol Chem 2000;275:36596-604.
64. Williams DL, de La Llera-Moya M, Thuahnai ST, Lund-Katz S, Connelly MA, Azhar S, Anantharamaiah GM, Phillips MC. Binding and cross-linking studies show that scavenger receptor BI interacts with multiple sites in apolipoprotein A-I and identify the class A amphipathic alpha-helix as a recognition motif. J Biol Chem 2000;275:18897-904.
65. Phillips MC. Molecular mechanisms of cellular cholesterol efflux. J Biol Chem 2014;289:24020-9.
66. Yamamoto S, Narita I, Kotani K. The macrophage and its related cholesterol efflux as a HDL function index in atherosclerosis. Clin Chim Acta 2016;457:117-22. 67. de la Llera-Moya M, Drazul-Schrader D, Asztalos BF, Cuchel M, Rader DJ, Rothblat GH. The ability to promote efflux via ABCA1 determines the capacity of serum specimens with similar high-density lipoprotein cholesterol to remove cholesterol from macrophages. Arterioscler Thromb Vasc Biol 2010;30:796-801. 68. Helal O, Berrougui H, Loued S, Khalil A. Extra-virgin olive oil consumption improves the capacity of HDL to mediate cholesterol efflux and increases ABCA1 and ABCG1 expression in human macrophages. Br J Nutr 2013;109:1844-55. 69. Saleheen D, Scott R, Javad S, Zhao W, Rodrigues A, Picataggi A,
Lukmanova D, Mucksavage ML, Luben R, Billheimer J, et al. Association of HDL cholesterol efflux capacity with incident coronary heart disease events: a
prospective case-control study. Lancet Diabetes Endocrinol 2015;3:507-13.
70. Li XM, Tang WH, Mosior MK, Huang Y, Wu Y, Matter W, Gao V, Schmitt D, Didonato JA, Fisher EA, et al. Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks. Arterioscler Thromb Vasc Biol 2013;33:1696-705.
71. Zhang J, Xu J, Wang J, Wu C, Xu Y, Wang Y, Deng F, Wang Z, Chen X, Wu M, et al. Prognostic Usefulness of Serum Cholesterol Efflux Capacity in Patients With Coronary Artery Disease. Am J Cardiol 2016;117:508-14.
72. Khera AV, Rader DJ. Cholesterol efflux capacity: full steam ahead or a bump in the road? Arterioscler Thromb Vasc Biol 2013;33:1449-51.
73. Bhatt A, Rohatgi A. HDL Cholesterol Efflux Capacity: Cardiovascular Risk Factor and Potential Therapeutic Target. Curr Atheroscler Rep 2016;18:2.
85
74. Hernáez Á, Fernández-Castillejo S, Farràs M, Catalán Ú, Subirana I,
Montes R, Solà R, Muñoz-Aguayo D, Gelabert-Gorgues A, Díaz-Gil Ó, et al. Olive oil polyphenols enhance high-density lipoprotein function in humans: a randomized controlled trial. Arterioscler Thromb Vasc Biol 2014;34:2115-9.
75. Montoya MT, Porres A, Serrano S, Fruchart JC, Mata P, Gerique JA, Castro GR. Fatty acid saturation of the diet and plasma lipid concentrations, lipoprotein particle concentrations, and cholesterol efflux capacity. Am J Clin Nutr
2002;75:484-91.
76. Blanco-Molina A, Castro G, Martín-Escalante D, Bravo D, López-Miranda J, Castro P, López-Segura F, Fruchart JC, Ordovás JM, Pérez-Jiménez F. Effects of different dietary cholesterol concentrations on lipoprotein plasma concentrations and on cholesterol efflux from Fu5AH cells. Am J Clin Nutr 1998;68:1028-33. 77. Sakr SW, Senault C, Vacher D, Fournier N, Girard-Globa A. Oleic acid-rich fats increase the capacity of postprandial serum to promote cholesterol efflux from Fu5AH cells. Biochim Biophys Acta 1996;1300:49-55.
78. Kralova Lesna I, Suchanek P, Kovar J, Stavek P, Poledne R. Replacement of dietary saturated FAs by PUFAs in diet and reverse cholesterol transport. J Lipid Res 2008;49:2414-8.
79. Buonacorso V, Nakandakare ER, Nunes VS, Passarelli M, Quintão EC, Lottenberg AM. Macrophage cholesterol efflux elicited by human total plasma and by HDL subfractions is not affected by different types of dietary fatty acids. Am J Clin Nutr 2007;86:1270-7.
80. De Vries R, Beusekamp BJ, Kerstens MN, Groen AK, Van Tol A, Dullaart RP. A low-saturated-fat, low-cholesterol diet decreases plasma CETP activity and pre beta-HDL formation but does not affect cellular cholesterol efflux to plasma from type 1 diabetic patients. Scand J Clin Lab Invest 2005;65:729-37.
81. Berryman CE, Grieger JA, West SG, Chen CY, Blumberg JB, Rothblat GH, Sankaranarayanan S, Kris-Etherton PM. Acute consumption of walnuts and walnut components differentially affect postprandial lipemia, endothelial function, oxidative stress, and cholesterol efflux in humans with mild hypercholesterolemia. J Nutr 2013;143:788-94.
82. Beulens JW, Sierksma A, van Tol A, Fournier N, van Gent T, Paul JL, Hendriks HF. Moderate alcohol consumption increases cholesterol efflux mediated by ABCA1. J Lipid Res 2004;45:1716-23.
83. Andersen CJ, Blesso CN, Lee J, Barona J, Shah D, Thomas MJ, Fernandez ML. Egg consumption modulates HDL lipid composition and increases the
cholesterol-accepting capacity of serum in metabolic syndrome. Lipids 2013;48:557-67.
84. Esteva O, Baudet MF, Lasserre M, Jacotot B. Influence of the fatty acid composition of high-density lipoprotein phospholipids on the cholesterol efflux from cultured fibroblasts. Biochim Biophys Acta 1986;875:174-82.
85. Weibel GL, Drazul-Schrader D, Shivers DK, Wade AN, Rothblat GH, Reilly MP, de la Llera-Moya M. Importance of evaluating cell cholesterol influx with efflux in determining the impact of human serum on cholesterol metabolism and
atherosclerosis. Arterioscler Thromb Vasc Biol 2014;34:17-25.
86. Sola R, Motta C, Maille M, Bargallo MT, Boisnier C, Richard JL, Jacotot B. Dietary monounsaturated fatty acids enhance cholesterol efflux from human
86
fibroblasts. Relation to fluidity, phospholipid fatty acid composition, overall composition, and size of HDL3. Arterioscler Thromb 1993;13:958-66.
87. Santé Canada. Fichier canadien sur les éléments nutritifs (FCÉN). Version 2015.
88. Serra-Majem L, Roman B, Estruch R. Scientific evidence of interventions using the Mediterranean diet: a systematic review. Nutr Rev 2006;64:S27-47. 89. Estruch R, Ros E, Salas-Salvadó J, Covas MI, Corella D, Arós F, Gómez- Gracia E, Ruiz-Gutiérrez V, Fiol M, Lapetra J, et al. Primary prevention of
cardiovascular disease with a Mediterranean diet. N Engl J Med 2013;368:1279- 90.
90. Escolà-Gil JC, Llaverias G, Julve J, Jauhiainen M, Méndez-González J, Blanco-Vaca F. The cholesterol content of Western diets plays a major role in the paradoxical increase in high-density lipoprotein cholesterol and upregulates the macrophage reverse cholesterol transport pathway. Arterioscler Thromb Vasc Biol 2011;31:2493-9.
91. Huth PJ, Fulgoni VL, Keast DR, Park K, Auestad N. Major food sources of calories, added sugars, and saturated fat and their contribution to essential nutrient intakes in the U.S. diet: data from the National Health and Nutrition Examination Survey (2003-2006). Nutr J 2013;12:116.
92. Drouin-Chartier J-P, Brassard D, Tessier-Grenier M, Côté JA, Labonté M-È, Desroches S, Couture P, Lamarche B. Systematic review of the association
between dairy product consumption and risk of cardiovascular-related clinical outcomes. Adv Nutr 2016;7:1026-40.