درشت مغذی‌ها و پاسخ‌های التهابی پس از جذب غذا در سندرم متابولیک: مروری بر شواهد موجود

نوع مقاله : مقاله مروری

نویسندگان

1 دانشجوی کارشناسی ارشد، کمیته‌ی تحقیقات دانشجویی، گروه تغذیه‌ی جامعه، دانشکده‌ی تغذیه و علوم غذایی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

2 دانشیار، مرکز تحقیقات امنیت غذایی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

چکیده

مقدمه: افزایش سطح بیومارکرهای التهابی پس از جذب غذا، محرکی در جهت شروع و پیشروی فرایندهای التهابی سیستمیک در بیماری‌های مزمن می‌باشد. به نظر می‌رسد فرایندهای التهابی مستقل از سطح لیپیدهای خونی موجب افزایش خطر بیماری‌های قلبی‌ عروقی و سندرم متابولیک می‌گردند. ترکیب درشت مغذی‌های رژیم غذایی به عنوان یکی از مهم‌ترین عوامل تعیین کننده‌ی موفقیت در کنترل فرایندهای التهابی در سندرم متابولیک مطرح شده است. هدف از بررسی حاضر، مروری بر پژوهش‌های انجام شده در زمینه‌ی درشت مغذی‌ها و پاسخ‌های التهابی پس از جذب غذا در سندرم متابولیک بود.روش‌ها: برای این منظور از جستجو در PubMed/Medline بین سال‌های 1970 تا 2011 با کلید واژه‌های Macronutrient، High/low-carbohydrate، Fat، Protein meal، postprandial/acute Inflammation، Endothelial function، Metabolic syndrome و هر یک از بیومارکرهای التهابی استفاده شد. مطالعات حیوانی و انسانی که به صورت مقطعی، آینده‌نگر و کارآزمایی‌های بالینی انجام شده بودند، در این مطالعه وارد شدند.یافته‌ها: دریافت درشت مغذی‌ها به ویژه دریافت کربوهیدرات در وعده‌ی غذایی منجر به افزایش سطح شاخص‌های التهابی پس از جذب غذا در افراد سالم و بیماران می‌گردد. در این میان به نظر می‌رسد بیشترین شدت و پایداری اثر بر فرایندهای استرس اکسیداتیو و پاسخ التهابی پس از جذب در میان درشت مغذی‌ها به کربوهیدرات رژیم غذایی اختصاص داشته باشد. پس از کربوهیدرات‌ها، چربی‌ها نیز بیش از پروتئین منجر به القای پاسخ التهابی پس از جذب غذا می‌شوند. در بین انواع چربی‌ها، مصرف ω3 در دوز بالا و MUFA (Monounsaturated fatty acid) با کاهش سطح سرمی‌ بیومارکرهای التهابی و آدیپوسیتوکین‌های پس از مصرف غذا همراه بود.نتیجه‌گیری: به نظر می‌رسد از میان درشت مغذی‌های رژیم غذایی، کربوهیدرات بیشترین نقش را در پیشروی عوامل خطر سنتی سندرم متابولیک و فرایندهای التهابی پس از غذا ایفا می‌نماید. با این وجود انجام تحقیقات بیشتر و نیز تعدیل نقایص طراحی مطالعات موجود، مؤید نتایج نهایی خواهد بود.

کلیدواژه‌ها


عنوان مقاله [English]

Macronutrients and Postprandial Inflammation in the Metabolic Syndrome: Review of Current Evidence

نویسندگان [English]

  • Somayeh Rajaie 1
  • Ahmad Esmaillzadeh 2
1 MSc Student, Student Research Committee, Department of Community Nutrition, School of Nutrition and Food Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
2 Associate Professor, Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
چکیده [English]

Background: Elevated postprandial inflammation accelerates the process of systemic inflammation involved in chronic diseases. It seems that inflammation promotes the risk of cardiovascular disease and metabolic syndrome (MetS) independent from the effect of blood lipids. Dietary macronutrient composition has been suggested as one of the most important determinants of inflammation in the MetS. This study aimed to review the current evidence on the effect of dietary macronutrients on postprandial inflammation in the MetS.Methods: We searched PubMed/Medline from 1970 until 2011 with macronutrient, high/low-carbohydrate,-fat,-protein meal, postprandial/acute inflammation, endothelial function, metabolic syndrome and individual inflammatory biomarkers as keywords. The cross-sectional and prospective studies as well as clinical trials were included in this investigation.Findings: Consumption of all dietary macronutrients, particularly dietary carbohydrates, was associated with elevated levels of postprandial inflammation in both healthy and unhealthy subjects. Carbohydrates have been consistently shown to induce postprandial inflammatory response as well as oxidative stress. Consumption of dietary fats has also been reported to result in increased levels of postprandial inflammation. However, the effects of dietary fats have been less than carbohydrates and more than dietary proteins. Of individual fatty acids, dietary intakes of MUFA (monounsaturated fatty acid) and high doses of ω3 fatty acids have been associated with reduced postprandial inflammation.Conclusion: Dietary intakes of carbohydrates, followed by dietary fats, are associated with elevated levels of postprandial inflammation. Further investigations are needed to confirm these conclusions. 

کلیدواژه‌ها [English]

  • Macronutrient
  • Carbohydrate
  • Fat
  • Protein
  • Inflammation
  • Metabolic Syndrome
  1. Grundy SM, Brewer HB, Jr., Cleeman JI, Smith SC, Jr., Lenfant C. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Arterioscler Thromb Vasc Biol 2004; 24(2): e13-e18.
  2. Mottillo S, Filion KB, Genest J, Joseph L, Pilote L, Poirier P, et al. The metabolic syndrome and cardiovascular risk a systematic review and meta-analysis. J Am Coll Cardiol 2010; 56(14): 1113-32.
  3. Esposito K, Giugliano D. Mediterranean diet and the metabolic syndrome: the end of the beginning. Metab Syndr Relat Disord 2010; 8(3): 197-200.
  4. Esmaillzadeh A, Azadbakht L. Dietary energy density and the metabolic syndrome among Iranian women. Eur J Clin Nutr 2011; 65(5): 598-605.
  5. Esmaillzadeh A, Mirmiran P, Azadbakht L, Etemadi A, Azizi F. High prevalence of the metabolic syndrome in Iranian adolescents. Obesity (Silver Spring) 2006; 14(3): 377-82.
  6. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic syndrome: a comprehensive perspective based on interactions between obesity, diabetes, and inflammation. Circulation 2005; 111(11): 1448-54.
  7. Esmaillzadeh A, Azadbakht L. Increased levels of inflammation among women with enlarged waist and elevated triglyceride concentrations. Ann Nutr Metab 2010; 57(2): 77-84.
  8. Williams KJ, Tabas I. Atherosclerosis and inflammation. Science 2002; 297(5581): 521-2.
  9. Koster A, Stenholm S, Alley DE, Kim LJ, Simonsick EM, Kanaya AM, et al. Body fat distribution and inflammation among obese older adults with and without metabolic syndrome. Obesity (Silver Spring) 2010; 18(12): 2354-61.
  10. Halkes CJ, van DH, de Jaegere PP, Plokker HW, van Der HY, Erkelens DW, et al. Postprandial increase of complement component 3 in normolipidemic patients with coronary artery disease: effects of expanded-dose simvastatin. Arterioscler Thromb Vasc Biol 2001; 21(9): 1526-30.
  11. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA 2007; 298(3): 309-16.
  12. Mora S, Rifai N, Buring JE, Ridker PM. Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events. Circulation 2008; 118(10): 993-1001.
  13. Klop B, Proctor SD, Mamo JC, Botham KM, Castro CM. Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases. Int J Vasc Med 2012; 2012: 947417.
  14. O'Keefe JH, Gheewala NM, O'Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol 2008; 51(3): 249-55.
  15. Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, et al. Differential effects of cream, glucose, and orange juice on inflammation, endotoxin, and the expression of Toll-like receptor-4 and suppressor of cytokine signaling-3. Diabetes Care 2010; 33(5): 991-7.
  16. Hlebowicz J, Darwiche G, Bjorgell O, Almer LO. Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects. Am J Clin Nutr 2007; 85(6): 1552-6.
  17. Aggarwal BB, Harikumar KB. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. Int J Biochem Cell Biol 2009; 41(1): 40-59.
  18. Dandona P, Ghanim H, Chaudhuri A, Dhindsa S, Kim SS. Macronutrient intake induces oxidative and inflammatory stress: potential relevance to atherosclerosis and insulin resistance. Exp Mol Med 2010; 42(4): 245-53.
  19. Fito M, Guxens M, Corella D, Saez G, Estruch R, de la Torre R, et al. Effect of a traditional Mediterranean diet on lipoprotein oxidation: a randomized controlled trial. Arch Intern Med 2007; 167(11): 1195-203.
  20. O'Keefe JH, Bell DS. Postprandial hyperglycemia/hyperlipidemia (postprandial dysmetabolism) is a cardiovascular risk factor. Am J Cardiol 2007; 100(5): 899-904.
  21. Volek JS, Feinman RD. Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond) 2005; 2: 31.
  22. Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER, III, et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA 2005; 294(19): 2455-64.
  23. Esmaillzadeh A, Azadbakht L. Different kinds of vegetable oils in relation to individual cardiovascular risk factors among Iranian women. Br J Nutr 2011; 105(6): 919-27.
  24. Rutter MK, Meigs JB, Sullivan LM, D'Agostino RB, Sr., Wilson PW. C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham Offspring Study. Circulation 2004; 110(4): 380-5.
  25. Shimabukuro M, Chinen I, Higa N, Takasu N, Yamakawa K, Ueda S. Effects of dietary composition on postprandial endothelial function and adiponectin concentrations in healthy humans: a crossover controlled study. Am J Clin Nutr 2007; 86(4): 923-8.
  26. Tsai WC, Li YH, Lin CC, Chao TH, Chen JH. Effects of oxidative stress on endothelial function after a high-fat meal. Clin Sci (Lond) 2004; 106(3): 315-9.
  27. Peake PW, Kriketos AD, Denyer GS, Campbell LV, Charlesworth JA. The postprandial response of adiponectin to a high-fat meal in normal and insulin-resistant subjects. Int J Obes Relat Metab Disord 2003; 27(6): 657-62.
  28. Lundman P, Boquist S, Samnegard A, Bennermo M, Held C, Ericsson CG, et al. A high-fat meal is accompanied by increased plasma interleukin-6 concentrations. Nutr Metab Cardiovasc Dis 2007; 17(3): 195-202.
  29. Esposito K, Ciotola M, Sasso FC, Cozzolino D, Saccomanno F, Assaloni R, et al. Effect of a single high-fat meal on endothelial function in patients with the metabolic syndrome: role of tumor necrosis factor-alpha. Nutr Metab Cardiovasc Dis 2007; 17(4): 274-9.
  30. Esposito K, Nappo F, Giugliano F, Di PC, Ciotola M, Barbieri M, et al. Meal modulation of circulating interleukin 18 and adiponectin concentrations in healthy subjects and in patients with type 2 diabetes mellitus. Am J Clin Nutr 2003; 78(6): 1135-40.
  31. Nappo F, Esposito K, Cioffi M, Giugliano G, Molinari AM, Paolisso G, et al. Postprandial endothelial activation in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals. J Am Coll Cardiol 2002; 39(7): 1145-50.
  32. Anderson JW, O'Neal DS, Riddell-Mason S, Floore TL, Dillon DW, Oeltgen PR. Postprandial serum glucose, insulin, and lipoprotein responses to high- and low-fiber diets. Metabolism 1995; 44(7): 848-54.
  33. Zampelas A, Peel AS, Gould BJ, Wright J, Williams CM. Polyunsaturated fatty acids of the n-6 and n-3 series: effects on postprandial lipid and apolipoprotein levels in healthy men. Eur J Clin Nutr 1994; 48(12): 842-8.
  34. Hodgson JM, Burke V, Beilin LJ, Puddey IB. Partial substitution of carbohydrate intake with protein intake from lean red meat lowers blood pressure in hypertensive persons. Am J Clin Nutr 2006; 83(4): 780-7.
  35. Elliott P, Stamler J, Dyer AR, Appel L, Dennis B, Kesteloot H, et al. Association between protein intake and blood pressure: the INTERMAP Study. Arch Intern Med 2006; 166(1): 79-87.
  36. Shah M, Adams-Huet B, Bantle JP, Henry RR, Griver KA, Raatz SK, et al. Effect of a high-carbohydrate versus a high--cis-monounsaturated fat diet on blood pressure in patients with type 2 diabetes. Diabetes Care 2005; 28(11): 2607-12.
  37. Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 2009; 44(4): 297-309.
  38. Tay J, Brinkworth GD, Noakes M, Keogh J, Clifton PM. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. J Am Coll Cardiol 2008; 51(1): 59-67.
  39. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA 2005; 293(1): 43-53.
  40. Yancy WS, Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004; 140(10): 769-77.
  41. Volek JS, Sharman MJ. Cardiovascular and hormonal aspects of very-low-carbohydrate ketogenic diets. Obes Res 2004; 12 Suppl 2: 115S-23S.
  42. Brehm BJ, Seeley RJ, Daniels SR, D'Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003; 88(4): 1617-23.
  43. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003; 348(21): 2082-90.
  44. Mandayam S, Mitch WE. Dietary protein restriction benefits patients with chronic kidney disease. Nephrology (Carlton ) 2006; 11(1): 53-7.
  45. Aljada A, Ghanim H, Mohanty P, Syed T, Bandyopadhyay A, Dandona P. Glucose intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase concentrations. Am J Clin Nutr 2004; 80(1): 51-7.
  46. Mohanty P, Hamouda W, Garg R, Aljada A, Ghanim H, Dandona P. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. J Clin Endocrinol Metab 2000; 85(8): 2970-3.
  47. Ajani UA, Ford ES, Mokdad AH. Dietary fiber and C-reactive protein: findings from national health and nutrition examination survey data. J Nutr 2004; 134(5): 1181-5.
  48. Blackburn P, Despres JP, Lamarche B, Tremblay A, Bergeron J, Lemieux I, et al. Postprandial variations of plasma inflammatory markers in abdominally obese men. Obesity (Silver Spring) 2006; 14(10): 1747-54.
  49. Manning PJ, Sutherland WH, Hendry G, de Jong SA, McGrath M, Williams SM. Changes in circulating postprandial proinflammatory cytokine concentrations in diet-controlled type 2 diabetes and the effect of ingested fat. Diabetes Care 2004; 27(10): 2509-11.
  50. Igarashi M, Hirata A, Yamauchi T, Yamaguchi H, Tsuchiya H, Ohnuma H, et al. Clinical utility and approach to estimate postprandial hypertriglycemia by a newly designed oral fat-loading test. J Atheroscler Thromb 2003; 10(5): 314-20.
  51. Carroll MF, Schade DS. Timing of antioxidant vitamin ingestion alters postprandial proatherogenic serum markers. Circulation 2003; 108(1): 24-31.
  52. Zahedi RG, Summers LK, Lumb P, Chik G, Crook MA. The response of serum sialic acid and other acute phase reactants to an oral fat load in healthy humans. Eur J Intern Med 2001; 12(6): 510-4.
  53. Dandona P, Aljada A, Mohanty P, Ghanim H, Hamouda W, Assian E, et al. Insulin inhibits intranuclear nuclear factor kappaB and stimulates IkappaB in mononuclear cells in obese subjects: evidence for an anti-inflammatory effect? J Clin Endocrinol Metab 2001; 86(7): 3257-65.
  54. Kelley DS. Modulation of human immune and inflammatory responses by dietary fatty acids. Nutrition 2001; 17(7-8): 669-73.
  55. Calder PC. Polyunsaturated fatty acids, inflammation, and immunity. Lipids 2001; 36(9): 1007-24.
  56. Rallidis LS, Paschos G, Liakos GK, Velissaridou AH, Anastasiadis G, Zampelas A. Dietary alpha-linolenic acid decreases C-reactive protein, serum amyloid A and interleukin-6 in dyslipidaemic patients. Atherosclerosis 2003; 167(2): 237-42.
  57. Ros E. Dietary cis-monounsaturated fatty acids and metabolic control in type 2 diabetes. Am J Clin Nutr 2003; 78(3 Suppl): 617S-25S.
  58. Baer DJ, Judd JT, Clevidence BA, Tracy RP. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study. Am J Clin Nutr 2004; 79(6): 969-73.
  59. Poppitt SD, Keogh GF, Lithander FE, Wang Y, Mulvey TB, Chan YK, et al. Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-alpha, and C-reactive protein to a high-fat dietary load. Nutrition 2008; 24(4): 322-9.
  60. Mohanty P, Ghanim H, Hamouda W, Aljada A, Garg R, Dandona P. Both lipid and protein intakes stimulate increased generation of reactive oxygen species by polymorphonuclear leukocytes and mononuclear cells. Am J Clin Nutr 2002; 75(4): 767-72.
  61. Aljada A, Mohanty P, Ghanim H, Abdo T, Tripathy D, Chaudhuri A, et al. Increase in intranuclear nuclear factor kappaB and decrease in inhibitor kappaB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Am J Clin Nutr 2004; 79(4): 682-90.
  62. Alipour A, Elte JW, van Zaanen HC, Rietveld AP, Cabezas MC. Postprandial inflammation and endothelial dysfuction. Biochem Soc Trans 2007; 35(Pt 3): 466-9.
  63. van Oostrom AJ, Alipour A, Plokker TW, Sniderman AD, Cabezas MC. The metabolic syndrome in relation to complement component 3 and postprandial lipemia in patients from an outpatient lipid clinic and healthy volunteers. Atherosclerosis 2007; 190(1): 167-73.
  64. Erridge C, Attina T, Spickett CM, Webb DJ. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. Am J Clin Nutr 2007; 86(5): 1286-92.