Kronik hastalıklar ekseninde diyette yüksek fruktoz ve doymuş yağ asitlerinin kronik düşük derece inflamasyon üzerine etkisi

Son yıllarda kronik hastalıkların ortaya çıkmasında, kronik düşük derece inflamasyonun rolü üzerinde durulmaktadır. Kronik düşük derece inflamasyon, sistemik dolaşım ve çeşitli dokularda inflamatuvar medyatörlerin ve bazı proinflamatuvar sitokinlerin artışı ile karakterize olan metabolik bir süreçtir. C reaktif protein (CRP), tümör nekrozis faktör-α (TNF-α), interlökin-1 (IL-1), interlökin-4 (IL-4), interlökin-6 (IL-6), toll benzeri reseptör-4 (TLR-4) kronik düşük derece inflamasyonda rol oynayan bazı proinflamatuvar moleküllerdir. Güncel çalışmalarda, hazır ve işlenmiş besinlerin tüketimiyle artan fruktoz ve doymuş yağ asitleri alımının kronik düşük derece inflamasyon oluşumunda etkileri olduğu gösterilmektedir. Bu derlemede, diyetle yüksek fruktoz ve doymuş yağ asitleri alımının, proinflamatuvar medyatörler aracılığıyla kronik düşük derece inflamasyon oluşumuna etkisi incelenmiştir.

Effects of dietary high fructose and saturated fatty acids on chronic low grade inflammation in the perspective of chronic diseases

In recent years, the role of chronic low grade inflammation in the emergence of chronic diseases has been emphasized. Chronic low grade inflammation is a metabolic process characterized by systemic circulation and increased inflammatory mediators and some proinflammatory cytokines in various tissues. C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), toll like receptor-4 (TLR-4) are some proinflammatory molecules that play a role in the chronic low grade inflammation. Recent studies have shown that fructose and saturated fatty acids, which are consumed with increased consumption of processed foods in the current diet, might trigger chronic low grade inflammation. In this review, the effects of dietary high fructose and saturated fatty acids on development of chronic low grade inflammation through some proinflammatory mediators were examined.

Keywords:

saturated fatty acid, fructose inflammation, proinflammatory molecules,

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1. World Health Organization. Global status report on noncommunicable diseases 2010. Geneva, WHO, 2010.
2. Velickovic N, Teofilovic A, Ilic D, Djordjevic A, Vojnovic Milutinovic D, Petrovic S et al. Modulation of hepatic inflammation and energy-sensing pathways in the rat liver by high-fructose diet and chronic stress. Eur J Nutr. 2018.
3. Zaki SM, Abdel Fattah S, Hassan DS. The differential effects of high-fat and high fructose diets on the liver of male albino rat and the proposed underlying mechanisms. Folia Morphol (Warsz). 2018.
4. Zitvogel L, Pietrocola F, Kroemer G. Nutrition, inflammation and cancer. Nat Immunol. 2017;18:843- 50.
5. Silveira BKS, Oliveira TMS, Andrade PA, Hermsdorff HHM, Rosa COB, Franceschini S. Dietary pattern and macronutrients profile on the variation of inflammatory biomarkers: scientific update. Cardiol Res Pract. 2018;2018:4762575.
6. Calder PC, Ahluwalia N, Albers R, Bosco N, BourdetSicard R, Haller D, et al. A consideration of biomarkers to be used for evaluation of inflammation in human nutritional studies. Br J Nutr. 2013;109l 1:S1-34.
7. Barbaresko J, Koch M, Schulze MB, Nothlings U. Dietary pattern analysis and biomarkers of low-grade inflammation: a systematic literature review. Nutr Rev. 2013;71(8):511-27.
8. Zhang DM, Jiao RQ, Kong LD. High dietary fructose: direct or indirect dangerous factors disturbing tissue and organ functions. Nutrients. 2017;9(4).
9. Nishida K, Otsu K. Inflammation and metabolic cardiomyopathy. Cardiovasc Res. 2017;113(4):389-98.
10. Kuzma JN, Cromer G, Hagman DK, Breymeyer KL, Roth CL, Foster-Schubert KE, et al. No differential effect of beverages sweetened with fructose, highfructose corn syrup, or glucose on systemic or adipose tissue inflammation in normal-weight to obese adults: a randomized controlled trial. Am J Clin Nutr. 2016;104(2):306-14.
11. Ruiz-Nunez B, Dijck-Brouwer DA, Muskiet FA. The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. J Nutr Biochem. 2016;36:1-20.
12. DiNicolantonio JJ, Lucan SC, O'Keefe JH. The evidence for saturated fat and for sugar related to coronary heart disease. Prog Cardiovasc Dis. 2016;58:464-72.
13. Ekici M, Kisa U, Arikan Durmaz S, Ugur E, NergizUnal R. Fatty acid transport receptor soluble CD36 and dietary fatty acid pattern in type 2 diabetic patients: a comparative study. Br J Nutr. 2018;119(2):153-62.
14. Calder PC, Ahluwalia N, Brouns F, Buetler T, Clement K, Cunningham K et al. Dietary factors and low-grade inflammation in relation to overweight and obesity. Br J Nutr. 2011;106 Suppl 3:S5-78.
15. Minihane AM, Vinoy S, Russell WR, Baka A, Roche HM, Tuohy KM, et al. Low-grade inflammation, diet composition and health: current research evidence and its translation. Br J Nutr. 2015;114(7):999-1012.
16. Calder PC, Albers R, Antoine JM, Blum S, BourdetSicard R, Ferns GA, et al. Inflammatory disease processes and interactions with nutrition. Br J Nutr. 2009;101:1-45.
17. Leon-Pedroza JI, Gonzalez-Tapia LA, del Olmo-Gil E, Castellanos-Rodriguez D, Escobedo G, GonzalezChavez A. [Low-grade systemic inflammation and the development of metabolic diseases: from the molecular evidence to the clinical practice]. Cir Cir. 2015;83:543-51.
18. Shivappa N, Bonaccio M, Hebert JR, Di Castelnuovo A, Costanzo S, Ruggiero E, et al. Association of proinflammatory diet with low-grade inflammation: results from the Molisani study. Nutrition. 2018;54:182-8.
19. Esser N, Legrand-Poels S, Piette J, Scheen AJ, Paquot N. Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. Diabetes Res Clin Pract. 2014;105:141-50.
20. Sun S, Ji Y, Kersten S, Qi L. Mechanisms of inflammatory responses in obese adipose tissue. Annu Rev Nutr. 2012;32:261-86.
21. Barbarroja N, Lopez-Pedrera R, Mayas MD, GarciaFuentes E, Garrido-Sanchez L, Macias-Gonzalez M et al. The obese healthy paradox: is inflammation the answer? Biochem J. 2010;430:141-9.
22. van Diepen JA, Berbee JF, Havekes LM, Rensen PC. Interactions between inflammation and lipid metabolism: relevance for efficacy of antiinflammatory drugs in the treatment of atherosclerosis. Atherosclerosis. 2013;228:306-15.
23. van Greevenbroek MM, Schalkwijk CG, Stehouwer CD. Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences. Neth J Med. 2013;71:174-87.
24. Baysal A. Beslenme. Ankara, Hatiboğlu Yayıncılık, 2012.
25. Makarem N, Bandera EV, Nicholson JM, Parekh N. Consumption of sugars, sugary foods, and sugary beverages in relation to cancer risk: a systematic review of longitudinal studies. Annu Rev Nutr. 2018.
26. Malik VS, Hu FB. Fructose and Cardiometabolic Health: What the Evidence From Sugar-Sweetened Beverages Tells Us. J Am Coll Cardiol. 2015;66:1615- 24.
27. Duffey KJ, Popkin BM. High-fructose corn syrup: is this what's for dinner? Am J Clin Nutr. 2008;88:1722- 32.
28. Dekker MJ, Su Q, Baker C, Rutledge AC, Adeli K. Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome. Am J Physiol Endocrinol Metab. 2010;299:E685-94.
29. Harvey RAPD. Lippincott's illustrated reviews: Biochemistry: Fifth edition. Philadelphia : Wolters Kluwer Health, 2011.
30. Hu FB, Malik VS. Sugar-sweetened beverages and risk of obesity and type 2 diabetes: epidemiologic evidence. Physiol Behav. 2010;100:47-54.
31. Kisioglu B, Nergiz-Unal R. Potential effect of maternal dietary sucrose or fructose syrup on CD36, leptin, and ghrelin-mediated fetal programming of obesity. Nutr Neurosci. 2018:1-11.
32. Yuruk AA, Nergiz-Unal R. Maternal dietary free or bound fructose diversely influence developmental programming of lipogenesis. Lipids Health Dis. 2017;16:226.
33. Choi Y, Abdelmegeed MA, Song BJ. Diet high in fructose promotes liver steatosis and hepatocyte apoptosis in C57BL/6J female mice: Role of disturbed lipid homeostasis and increased oxidative stress. Food Chem Toxicol. 2017;103:111-21.
34. Porto ML, Lirio LM, Dias AT, Batista AT, Campagnaro BP, Mill JG et al. Increased oxidative stress and apoptosis in peripheral blood mononuclear cells of fructose-fed rats. Toxicol In Vitro. 2015;29:1977-81.
35. Sanchez-Lozada LG, Mu W, Roncal C, Sautin YY, Abdelmalek M, Reungjui S et al. Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver. Eur J Nutr. 2010;49:1-9.
36. Baena M, Sanguesa G, Hutter N, Sanchez RM, Roglans N, Laguna JC et al. Fructose supplementation impairs rat liver autophagy through mTORC activation without inducing endoplasmic reticulum stress. Biochim Biophys Acta. 2015;1851:107-16.
37. Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC et al. Circulating concentrations of monocyte chemoattractant protein1, plasminogen activator inhibitor-1, and soluble leukocyte adhesion molecule-1 in overweight/obese men and women consuming fructose- or glucosesweetened beverages for 10 weeks. J Clin Endocrinol Metab. 2011;96:E2034-8.
38. Johnston RD, Stephenson MC, Crossland H, Cordon SM, Palcidi E, Cox EF et al. No difference between high-fructose and high-glucose diets on liver triacylglycerol or biochemistry in healthy overweight men. Gastroenterology. 2013;145:1016-25 e2.
39. Aeberli I, Gerber PA, Hochuli M, Kohler S, Haile SR, Gouni-Berthold I et al. Low to moderate sugarsweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial. Am J Clin Nutr. 2011;94:479-85.
40. Lee JH. Polyunsaturated Fatty acids in children. Pediatr Gastroenterol Hepatol Nutr. 2013;16:153-61.
41. Hacettepe Üniversitesi Beslenme ve Diyetetik Bölümü. Türkiye'ye Özgü Besin ve Beslenme Rehberi. Temmuz 2015.
42. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition Report of an expert consultation. 2010.
43. Fritsche KL. The science of fatty acids and inflammation. Adv Nutr. 2015;6:293-301.
44. Teeman CS, Kurti SP, Cull BJ, Emerson SR, Haub MD, Rosenkranz SK. Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise. Nutr Metab (Lond). 2016;13:80.
45. Nergiz-Unal R. Diyet yağı ve yağ asitleriyle immün sistem etkileşimi. Turkiye Klinikleri J Nutr Diet. 2016;2:32-5.
46. Enos RT, Davis JM, Velazquez KT, McClellan JL, Day SD, Carnevale KA, et al. Influence of dietary saturated fat content on adiposity, macrophage behavior, inflammation, and metabolism: composition matters. J Lipid Res. 2013;54:152-63.
47. Enos RT, Velazquez KT, Murphy EA. Insight into the impact of dietary saturated fat on tissue-specific cellular processes underlying obesity-related diseases. J Nutr Biochem. 2014;25:600-12.
48. Suganami T, Tanimoto-Koyama K, Nishida J, Itoh M, Yuan X, Mizuarai S et al. Role of the Toll-like receptor 4/NF-kappaB pathway in saturated fatty acid-induced inflammatory changes in the interaction between adipocytes and macrophages. Arterioscler Thromb Vasc Biol. 2007;27:84-91.
49. Sui YH, Luo WJ, Xu QY, Hua J. Dietary saturated fatty acid and polyunsaturated fatty acid oppositely affect hepatic NOD-like receptor protein 3 inflammasome through regulating nuclear factorkappa B activation. World J Gastroenterol. 2016;22:2533-44.
50. Milanski M, Degasperi G, Coope A, Morari J, Denis R, Cintra DE et al. Saturated fatty acids produce an inflammatory response predominantly through the activation of TLR4 signaling in hypothalamus: implications for the pathogenesis of obesity. J Neurosci. 2009;29:359-70.
51. King DE, Egan BM, Geesey ME. Relation of dietary fat and fiber to elevation of C-reactive protein. The American Journal of Cardiology. 2003;92:1335-9.
52. Marina A, von Frankenberg AD, Suvag S, Callahan HS, Kratz M, Richards TL et al. Effects of dietary fat and saturated fat content on liver fat and markers of oxidative stress in overweight/obese men and women under weight-stable conditions. Nutrients. 2014;6:4678-90.
53. Teng KT, Chang LF, Vethakkan SR, Nesaretnam K, Sanders TAB. Effects of exchanging carbohydrate or monounsaturated fat with saturated fat on inflammatory and thrombogenic responses in subjects with abdominal obesity: A randomized controlled trial. Clin Nutr. 2017;36:1250-8.
54. Peairs AD, Rankin JW, Lee YW. Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults. Nutr J. 2011;10:122.
55. Angelopoulos TJ, Lowndes J, Sinnett S, Rippe JM. Fructose containing sugars at normal levels of consumption do not effect adversely components of the metabolic syndrome and risk factors for cardiovascular disease. Nutrients. 2016;8:179.
56. Jin R, Welsh JA, Le NA, Holzberg J, Sharma P, Martin DR, et al. Dietary fructose reduction improves markers of cardiovascular disease risk in HispanicAmerican adolescents with NAFLD. Nutrients. 2014;6:3187-201.
57. Johnson LK, Holven KB, Nordstrand N, Mellembakken JR, Tanbo T, Hjelmesaeth J. Fructose content of low calorie diets: effect on cardiometabolic risk factors in obese women with polycystic ovarian syndrome: a randomized controlled trial. Endocr Connect. 2015;4:144-54.
58. Lowndes J, Sinnett S, Yu Z, Rippe J. The effects of fructose-containing sugars on weight, body composition and cardiometabolic risk factors when consumed at up to the 90th percentile population consumption level for fructose. Nutrients. 2014;6:3153-68.
59. Raatz SK, Johnson LK, Picklo MJ. Consumption of honey, sucrose, and high-fructose corn syrup produces similar metabolic effects in glucose-tolerant and -intolerant individuals. J Nutr. 2015;145:2265-72.
60. Silbernagel G, Machann J, Haring HU, Fritsche A, Peter A. Plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, e-selectin and C-reactive protein levels in response to 4-week very-highfructose or -glucose diets. Eur J Clin Nutr. 2014;68:97-100.
61. Yaghoobi N, Al-Waili N, Ghayour-Mobarhan M, Parizadeh SM, Abasalti Z, Yaghoobi Z et al. Natural honey and cardiovascular risk factors; effects on blood glucose, cholesterol, triacylglycerole, CRP, and body weight compared with sucrose. ScientificWorldJournal. 2008;8:463-9.
62. Kalogeropoulos N, Panagiotakos DB, Pitsavos C, Chrysohoou C, Rousinou G, Toutouza M et al. Unsaturated fatty acids are inversely associated and n6/n-3 ratios are positively related to inflammation and coagulation markers in plasma of apparently healthy adults. Clin Chim Acta. 2010;411:584-91.
63. Murakami K, Sasaki S, Takahashi Y, Uenishi K, Yamasaki M, Hayabuchi H et al. Total n-3 polyunsaturated fatty acid intake is inversely associated with serum C-reactive protein in young Japanese women. Nutr Res. 2008;28:309-14.
64. Bo S, Ciccone G, Guidi S, Gambino R, Durazzo M, Gentile L et al. Diet or exercise: what is more effective in preventing or reducing metabolic alterations? Eur J Endocrinol. 2008;159:685-91.
65. Petersson H, Lind L, Hulthe J, Elmgren A, Cederholm T, Riserus U. Relationships between serum fatty acid composition and multiple markers of inflammation and endothelial function in an elderly population. Atherosclerosis. 2009;203:298-303.
66. 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;79:969-73.
67. Santos S, Oliveira A, Casal S, Lopes C. Saturated fatty acids intake in relation to C-reactive protein, adiponectin, and leptin: a population-based study. Nutrition. 2013;29:892-7