سندرم متابولیک و کبد چرب غیر الکلی: رویکرد تغذیه‌ای در پیشگیری

نوع مقاله : مقاله مروری

نویسندگان

1 دانشیار، گروه تغذیه‌ی بالینی، دانشکده‌ی تغذیه و علوم غذایی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

2 کارشناس، گروه تغذیه، دانشکده‌ی تغذیه و علوم غذایی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

چکیده

مقدمه: سندرم متابولیک مجموعه‌ای از عوامل خطرزای متابولیک است که در یک فرد وجود دارند. این عوامل خطرزا شامل مقاومت به انسولین، فشار خون، اختلالات چربی خون و افزایش خطر انعقاد می‌باشند. اغلب بیماران دچار اضافه وزن یا چاقی می‌باشند و برخی از آن‌ها از کبد چرب رنج می‌برند. این نکته ارتباط قوی کبد چرب را با سندرم متابولیک نشان می‌دهد. هدف مطالعه‌ی حاضر، خلاصه کردن شواهد موجود در زمینه‌ی اپیدمیولوژی، پاتوفیزیولوژی کبد چرب غیر الکلی و سندرم متابولیک و یافته‌های مبنی بر اثرات مقدار ماده‌ی مغذی یا اجزای خاص غذایی (مانند اسید چرب امگا 3) بود.روش‌ها: به این منظور واژگان کلیدی “Metabolic syndrome”، “Nonalcoholic Fatty Liver”،  “Metabolic syndrome and diet”، “Metabolic syndrome and Nonalcoholic Fatty Liver”، “Nonalcoholic Fatty Liver and diet”، “Nonalcoholic Fatty Liver and nutrition” و “Metabolic syndrome and nutrition” در PubMed و EMBASE بین سال‌های 1998 تا 2013 جستجو کردیم.یافته‌ها: افزایش جهانی شیوع چاقی با افزایش شیوع کبد چرب غیر الکلی و همچنین افزایش خطر دیابت نوع 2 همراه است. اگر چه راهکار خاصی برای درمان کبد چرب غیر الکلی وجود ندارد، ولی اصلاح رژیم غذایی نقش خاصی در درمان آن دارد. الگوهای غذایی سرشار از میوه و سبزیجات همراه با شیوع کمتری از سندرم متابولیک بودند. دریافت زیاد گوشت با اجزای سندرم متابولیک به ویژه اختلال در تحمل گلوکز همراه بود. دریافت اسیدهای چرب ترانس از روغن‌های هیدروژنه با افزایش مارکرهای التهابی همراه بوده است. به نظر می‌رسد یک رژیم غذایی حاوی مقادیر کم کربوهیدرات و اسید چرب اشباع و مقدار بیشتر فیبر و اسیدهای چرب امگا 3 برای کنترل سندرم متابولیک مفید باشد. پیشنهاد می‌شود در مبتلایان کبد چرب غیر الکلی، دریافت غذاها و نوشیدنی‌های سرشار از فروکتوز محدود شود. یافته‌ها ارتباط معکوس بین مصرف قهوه و سندرم متابولیک را به دلیل شیوع کمتر هیپر تری‌گلیسریدمی نشان داد و پیشنهاد شده است که دریافت قهوه می‌تواند خطر کبد چرب غیر الکلی را کاهش دهد.نتیجه‌گیری: برنامه‌ای مبنی بر کاهش وزن تدریجی و فعالیت فیزیکی، هنوز یک استاندارد طلایی درمان کبد چرب غیر الکلی می‌شود. مصرف منظم میوه و سیبزیجات برای کاهش خطر ایجاد سندرم متابولیک پیشنهاد می‌شود.

کلیدواژه‌ها


عنوان مقاله [English]

Metabolic Syndrome and Nonalcoholic Fatty Liver Disease: Nutritional Approach for Prevention

نویسندگان [English]

  • Zamzam Paknahad 1
  • Hadi Zeraei-Bidgoli 2
1 Associate Professor, Department of Clinical Nutrition, School of Nutrition, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Nutrition School of Nutrition, Isfahan University of Medical Sciences, Isfahan, Iran
چکیده [English]

Background: Metabolic syndrome is a cluster of metabolic risk factors that come together in a single individual. These metabolic factors include insulin resistance, hypertension (high blood pressure), dyslipidemia, and an increased risk for clotting. Patients are most often overweight or obese. The development of nonalcoholic fatty liver disease (NAFLD) is strongly associated with the metabolic syndrome as reflected by the fact that most of the patients with NAFLD have more than one feature of metabolic syndrome. The aim of this review was to summarize the current knowledge on the epidemiology and pathophysiology of both NAFLD and metabolic syndrome and the findings about the effects nutrient content or specific food components (such as ω3 fatty acids).Methods: We searched Pubmed, ISI web of science, and EMBASE databases by using “Metabolic syndrome’, ‘Nonalcoholic fatty liver” , “Metabolic syndrome & diet”, “Metabolic syndrome & nonalcoholic fatty liver”, ‘Nonalcoholic fatty liver & diet” , “Nonalcoholic fatty liver & nutrition”, and “Metabolic syndrome & nutrition” from 2008 until 2013.Findings: The global increase in the prevalence of obesity is associated with NAFLD. NAFLD is also commonly associated with an increased risk of Type 2 diabetes mellitus development. Although there are no ideal options available for NAFLD treatment, dietary modification has a major role. Dietary patterns highly in fruit and vegetable content were generally found to be associated with lower prevalence of metabolic syndrome. High meat intake was associated with components of metabolic syndrome, especially impaired glucose tolerance. Intake of trans fatty acids from hydrogenated oils found to increase inflammatory markers. A low carbohydrate and saturated fat and high fiber and ω3 fatty acid diet is likely to be beneficial. The higher intake of soft drinks is associated with an increased risk of NAFLD. It is recommended to limit the intake of high-fructose foods and beverages in the NAFLD population. Findings showed negative correlation between coffee consumption and metabolic syndrome, because of the lower prevalence of hypertriglyceridemia, and data suggested coffee intake can reduce the risk of NAFLD.Conclusion: A gradual weight reduction and physical activity program is still the gold standard of NAFLD treatment. Regular consumption of fruit and vegetables is recommended to reduce the risk of developing metabolic syndrome.

کلیدواژه‌ها [English]

  • Metabolic Syndrome
  • Nonalcoholic fatty liver disease (NAFLD)
  • Diet
  • Nutrition
  1. Grundy SM. Metabolic syndrome scientific statement by the American Heart Association and the National Heart, Lung, and Blood Institute. Arterioscler Thromb Vasc Biol 2005; 25(11): 2243-4.
  2. Reynolds K, He J. Epidemiology of the metabolic syndrome. Am J Med Sci 2005; 330(6): 273-9.
  3. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106(25): 3143-421.
  4. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005; 112(17): 2735-52.
  5. Afkhami-Ardekani M, Zahedi-Asl S, Rashidi M, Atifah M, Hosseinpanah F, Azizi F. Incidence and trend of a metabolic syndrome phenotype among Tehranian adolescents: findings from the Tehran Lipid and Glucose Study, 1998-2001 to 2003-2006. Diabetes Care 2010; 33(9): 2110-2.
  6. Heidari R, Sadeghi M, Talaei M, Rabiei K, Mohammadifard N, Sarrafzadegan N. Metabolic syndrome in menopausal transition: Isfahan Healthy Heart Program, a population based study. Diabetol Metab Syndr 2010; 2: 59.
  7. Athyros VG, Bouloukos VI, Pehlivanidis AN, Papageorgiou AA, Dionysopoulou SG, Symeonidis AN, et al. The prevalence of the metabolic syndrome in Greece: the MetS-Greece Multicentre Study. Diabetes Obes Metab 2005; 7(4): 397-405.
  8. Yki-Jarvinen H. Nutritional modulation of nonalcoholic fatty liver disease and insulin resistance: human data. Curr Opin Clin Nutr Metab Care 2010; 13(6): 709-14.
  9. Hubscher SG. Histological assessment of non-alcoholic fatty liver disease. Histopathology 2006; 49(5): 450-65.
  10. Kleiner DE, Brunt EM, Van NM, Behling C, Contos MJ, Cummings OW, et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology 2005; 41(6): 1313-21.
  11. Wilkins T, Tadkod A, Hepburn I, Schade RR. Nonalcoholic fatty liver disease: diagnosis and management. Am Fam Physician 2013; 88(1): 35-42.
  12. Adams LA, Lindor KD. Nonalcoholic fatty liver disease. Ann Epidemiol 2007; 17(11): 863-9.
  13. Duvnjak M, Lerotic I, Barsic N, Tomasic V, Virovic JL, Velagic V. Pathogenesis and management issues for non-alcoholic fatty liver disease. World J Gastroenterol 2007; 13(34): 4539-50.
  14. Setji TL, Holland ND, Sanders LL, Pereira KC, Diehl AM, Brown AJ. Nonalcoholic steatohepatitis and nonalcoholic Fatty liver disease in young women with polycystic ovary syndrome. J Clin Endocrinol Metab 2006; 91(5): 1741-7.
  15. Adams LA, Lymp JF, St SJ, Sanderson SO, Lindor KD, Feldstein A, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005; 129(1): 113-21.
  16. Bedogni G, Miglioli L, Masutti F, Tiribelli C, Marchesini G, Bellentani S. Prevalence of and risk factors for nonalcoholic fatty liver disease: the Dionysos nutrition and liver study. Hepatology 2005; 42(1): 44-52.
  17. Mohammadifard N, Paknahad Z, Sajadi F, Maghroon M, Safari H, Ghasemi AR, et al. Relationship between obesity and cardiovascular risk factors in adults living in central Iran: results of Isfahan Healthy Heart Program. Iran J Nutr Sci Food Technol 2009; 3(4): 19-28. [In Persian].
  18. Noroozi M, Rastegari Z, Paknahad Z. Type of body fat distribution in postmenopausal women and its related factors. Iran J Nurs Midwifery Res 2010; 15(1): 27-31.
  19. Noroozi M, Paknahad Z, Taebi M. Factors associated with waist circumference of women in Isfahan. Behbood J 2004; 8(4): 31-40. [In Persian].
  20. Donnelly KL, Smith CI, Schwarzenberg SJ, Jessurun J, Boldt MD, Parks EJ. Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. J Clin Invest 2005; 115(5): 1343-51.
  21. Gupte P, Amarapurkar D, Agal S, Baijal R, Kulshrestha P, Pramanik S, et al. Non-alcoholic steatohepatitis in type 2 diabetes mellitus. J Gastroenterol Hepatol 2004; 19(8): 854-8.
  22. Ekstedt M, Franzen LE, Mathiesen UL, Thorelius L, Holmqvist M, Bodemar G, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006; 44(4): 865-73.
  23. Marchesini G, Bugianesi E, Forlani G, Cerrelli F, Lenzi M, Manini R, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 2003; 37(4): 917-23.
  24. Marchesini G, Marzocchi R. Metabolic syndrome and NASH. Clin Liver Dis 2007; 11(1): 105-17, ix.
  25. Donati G, Stagni B, Piscaglia F, Venturoli N, Morselli-Labate AM, Rasciti L, et al. Increased prevalence of fatty liver in arterial hypertensive patients with normal liver enzymes: role of insulin resistance. Gut 2004; 53(7): 1020-3.
  26. Hsiao PJ, Kuo KK, Shin SJ, Yang YH, Lin WY, Yang JF, et al. Significant correlations between severe fatty liver and risk factors for metabolic syndrome. J Gastroenterol Hepatol 2007; 22(12): 2118-23.
  27. Hamaguchi M, Kojima T, Takeda N, Nakagawa T, Taniguchi H, Fujii K, et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med 2005; 143(10): 722-8.
  28. Kotronen A, Westerbacka J, Bergholm R, Pietilainen KH, Yki-Jarvinen H. Liver fat in the metabolic syndrome. J Clin Endocrinol Metab 2007; 92(9): 3490-7.
  29. Speliotes EK, Massaro JM, Hoffmann U, Vasan RS, Meigs JB, Sahani DV, et al. Fatty liver is associated with dyslipidemia and dysglycemia independent of visceral fat: the Framingham Heart Study. Hepatology 2010; 51(6): 1979-87.
  30. Kim LJ, Nalls MA, Eiriksdottir G, Sigurdsson S, Launer LJ, Koster A, et al. Associations of visceral and liver fat with the metabolic syndrome across the spectrum of obesity: the AGES-Reykjavik study. Obesity (Silver Spring) 2011; 19(6): 1265-71.
  31. Tominaga K, Fujimoto E, Suzuki K, Hayashi M, Ichikawa M, Inaba Y. Prevalence of non-alcoholic fatty liver disease in children and relationship to metabolic syndrome, insulin resistance, and waist circumference. Environ Health Prev Med 2009; 14(2): 142-9.
  32. Kelishadi R, Cook SR, Adibi A, Faghihimani Z, Ghatrehsamani S, Beihaghi A, et al. Association of the components of the metabolic syndrome with non-alcoholic fatty liver disease among normal-weight, overweight and obese children and adolescents. Diabetol Metab Syndr 2009; 1: 29.
  33. Chiang PH, Chang TY, Chen JD. Synergistic effect of fatty liver and smoking on metabolic syndrome. World J Gastroenterol 2009; 15(42): 5334-9.
  34. Page J. Nonalcoholic fatty liver disease: the hepatic metabolic syndrome. J Am Acad Nurse Pract 2012; 24(6): 345-51.
  35. de LC, Olefsky JM. Inflammation and insulin resistance. FEBS Lett 2008; 582(1): 97-105.
  36. McCullough AJ. Pathophysiology of nonalcoholic steatohepatitis. J Clin Gastroenterol 2006; 40(Suppl 1): S17-S29.
  37. Taniguchi CM, Emanuelli B, Kahn CR. Critical nodes in signalling pathways: insights into insulin action. Nat Rev Mol Cell Biol 2006; 7(2): 85-96.
  38. Dowman JK, Tomlinson JW, Newsome PN. Pathogenesis of non-alcoholic fatty liver disease. QJM 2010; 103(2): 71-83.
  39. Sanyal AJ. Mechanisms of Disease: pathogenesis of nonalcoholic fatty liver disease. Nat Clin Pract Gastroenterol Hepatol 2005; 2(1): 46-53.
  40. Nielsen S, Guo Z, Johnson CM, Hensrud DD, Jensen MD. Splanchnic lipolysis in human obesity. J Clin Invest 2004; 113(11): 1582-8.
  41. Madan K, Bhardwaj P, Thareja S, Gupta SD, Saraya A. Oxidant stress and antioxidant status among patients with nonalcoholic fatty liver disease (NAFLD). J Clin Gastroenterol 2006; 40(10): 930-5.
  42. Qureshi K, Abrams GA. Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease. World J Gastroenterol 2007; 13(26): 3540-53.
  43. Paterson JM, Morton NM, Fievet C, Kenyon CJ, Holmes MC, Staels B, et al. Metabolic syndrome without obesity: Hepatic overexpression of 11beta-hydroxysteroid dehydrogenase type 1 in transgenic mice. Proc Natl Acad Sci U S A 2004; 101(18): 7088-93.
  44. Wei Y, Rector RS, Thyfault JP, Ibdah JA. Nonalcoholic fatty liver disease and mitochondrial dysfunction. World J Gastroenterol 2008; 14(2): 193-9.
  45. Chalasani N, Gorski JC, Asghar MS, Asghar A, Foresman B, Hall SD, et al. Hepatic cytochrome P450 2E1 activity in nondiabetic patients with nonalcoholic steatohepatitis. Hepatology 2003; 37(3): 544-50.
  46. Schattenberg JM, Wang Y, Singh R, Rigoli RM, Czaja MJ. Hepatocyte CYP2E1 overexpression and steatohepatitis lead to impaired hepatic insulin signaling. J Biol Chem 2005; 280(11): 9887-94.
  47. Poli G. Pathogenesis of liver fibrosis: role of oxidative stress. Mol Aspects Med 2000; 21(3): 49-98.
  48. Rector RS, Thyfault JP, Wei Y, Ibdah JA. Non-alcoholic fatty liver disease and the metabolic syndrome: an update. World J Gastroenterol 2008; 14(2): 185-92.
  49. Assy N, Nassar F, Nasser G, Grosovski M. Olive oil consumption and non-alcoholic fatty liver disease. World J Gastroenterol 2009; 15(15): 1809-15.
  50. Baxter AJ, Coyne T, McClintock C. Dietary patterns and metabolic syndrome--a review of epidemiologic evidence. Asia Pac J Clin Nutr 2006; 15(2): 134-42.
  51. McNaughton SA, Ball K, Mishra GD, Crawford DA. Dietary patterns of adolescents and risk of obesity and hypertension. J Nutr 2008; 138(2): 364-70.
  52. Mikkila V, Rasanen L, Raitakari OT, Marniemi J, Pietinen P, Ronnemaa T, et al. Major dietary patterns and cardiovascular risk factors from childhood to adulthood. The Cardiovascular Risk in Young Finns Study. Br J Nutr 2007; 98(1): 218-25.
  53. Steffen LM, Jacobs DR, Jr., Murtaugh MA, Moran A, Steinberger J, Hong CP, et al. Whole grain intake is associated with lower body mass and greater insulin sensitivity among adolescents. Am J Epidemiol 2003; 158(3): 243-50.
  54. Yannakoulia M, Yiannakouris N, Melistas L, Kontogianni MD, Malagaris I, Mantzoros CS. A dietary pattern characterized by high consumption of whole-grain cereals and low-fat dairy products and low consumption of refined cereals is positively associated with plasma adiponectin levels in healthy women. Metabolism 2008; 57(6): 824-30.
  55. Qi L, van Dam RM, Liu S, Franz M, Mantzoros C, Hu FB. Whole-grain, bran, and cereal fiber intakes and markers of systemic inflammation in diabetic women. Diabetes Care 2006; 29(2): 207-11.
  56. Azadbakht L, Farajian S, Barak F, Mir Aghajani M, Sarrafzadegan N, Esmaeilzadeh A. The relationship of red meat intake with metabolic syndrome and CRP plasma concentration in women. J Health Syst Res 2010; 6(4): 666-75. [In Persian].
  57. Zemel MB, Richards J, Milstead A, Campbell P. Effects of calcium and dairy on body composition and weight loss in African-American adults. Obes Res 2005; 13(7): 1218-25.
  58. Pereira MA, Jacobs DR, Jr., Van HL, Slattery ML, Kartashov AI, Ludwig DS. Dairy consumption, obesity, and the insulin resistance syndrome in young adults: the CARDIA Study. JAMA 2002; 287(16): 2081-9.
  59. Bazzano LA, He J, Ogden LG, Loria CM, Vupputuri S, Myers L, et al. Fruit and vegetable intake and risk of cardiovascular disease in US adults: the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Am J Clin Nutr 2002; 76(1): 93-9.
  60. Alonso A, de la Fuente C, Martin-Arnau AM, de IJ, Martinez JA, Martinez-Gonzalez MA. Fruit and vegetable consumption is inversely associated with blood pressure in a Mediterranean population with a high vegetable-fat intake: the Seguimiento Universidad de Navarra (SUN) Study. Br J Nutr 2004; 92(2): 311-9.
  61. Rolls BJ, Ello-Martin JA, Tohill BC. What can intervention studies tell us about the relationship between fruit and vegetable consumption and weight management? Nutr Rev 2004; 62(1): 1-17.
  62. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation 2008; 117(6): 754-61.
  63. Williams DE, Prevost AT, Whichelow MJ, Cox BD, Day NE, Wareham NJ. A cross-sectional study of dietary patterns with glucose intolerance and other features of the metabolic syndrome. Br J Nutr 2000; 83(3): 257-66.
  64. Samaha FF. Effect of very high-fat diets on body weight, lipoproteins, and glycemic status in the obese. Curr Atheroscler Rep 2005; 7(6): 412-20.
  65. Pelkman CL, Fishell VK, Maddox DH, Pearson TA, Mauger DT, Kris-Etherton PM. Effects of moderate-fat (from monounsaturated fat) and low-fat weight-loss diets on the serum lipid profile in overweight and obese men and women. Am J Clin Nutr 2004; 79(2): 204-12.
  66. Lottenberg AM. Importance of the dietary fat on the prevention and control of metabolic disturbances and cardiovascular disease. Arq Bras Endocrinol Metabol 2009; 53(5): 595-607.
  67. Kris-Etherton PM, Grieger JA, Etherton TD. Dietary reference intakes for DHA and EPA. Prostaglandins Leukot Essent Fatty Acids 2009; 81(2-3): 99-104.
  68. Zuchi C, Ambrosio G, Luscher TF, Landmesser U. Nutraceuticals in cardiovascular prevention: lessons from studies on endothelial function. Cardiovasc Ther 2010; 28(4): 187-201.
  69. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 2010; 91(3): 502-9.
  70. Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 1998; 98(12): 1198-204.
  71. Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005; 63(5): 133-57.
  72. Ferder L, Ferder MD, Inserra F. The role of high-fructose corn syrup in metabolic syndrome and hypertension. Curr Hypertens Rep 2010; 12(2): 105-12.
  73. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation 2007; 116(5): 480-8.
  74. Hosseini-Esfahani F, Bahadoran Z, Mirmiran P, Hosseinpour-Niazi S, Hosseinpanah F, Azizi F. Dietary fructose and risk of metabolic syndrome in adults: Tehran Lipid and Glucose study. Nutr Metab (Lond) 2011; 8(1): 50.
  75. Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension 2003; 41(6): 1183-90.
  76. Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007; 86(4): 899-906.
  77. Ruggiero C, Cherubini A, Ble A, Bos AJ, Maggio M, Dixit VD, et al. Uric acid and inflammatory markers. Eur Heart J 2006; 27(10): 1174-81.
  78. Quiroz Y, Pons H, Gordon KL, Rincon J, Chavez M, Parra G, et al. Mycophenolate mofetil prevents salt-sensitive hypertension resulting from nitric oxide synthesis inhibition. Am J Physiol Renal Physiol 2001; 281(1): F38-F47.
  79. Choi JW, Ford ES, Gao X, Choi HK. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2008; 59(1): 109-16.
  80. Gao X, Qi L, Qiao N, Choi HK, Curhan G, Tucker KL, et al. Intake of added sugar and sugar-sweetened drink and serum uric acid concentration in US men and women. Hypertension 2007; 50(2): 306-12.
  81. Ricci-Cabello I, Herrera MO, Artacho R. Possible role of milk-derived bioactive peptides in the treatment and prevention of metabolic syndrome. Nutr Rev 2012; 70(4): 241-55.
  82. Koteish A, Diehl AM. Animal models of steatosis. Semin Liver Dis 2001; 21(1): 89-104.
  83. Shah K, Stufflebam A, Hilton TN, Sinacore DR, Klein S, Villareal DT. Diet and exercise interventions reduce intrahepatic fat content and improve insulin sensitivity in obese older adults. Obesity (Silver Spring) 2009; 17(12): 2162-8.
  84. Katan MB. Weight-loss diets for the prevention and treatment of obesity. N Engl J Med 2009; 360(9): 923-5.
  85. Heath RB, Karpe F, Milne RW, Burdge GC, Wootton SA, Frayn KN. Selective partitioning of dietary fatty acids into the VLDL TG pool in the early postprandial period. J Lipid Res 2003; 44(11): 2065-72.
  86. Westerbacka J, Lammi K, Hakkinen AM, Rissanen A, Salminen I, Aro A, et al. Dietary fat content modifies liver fat in overweight nondiabetic subjects. J Clin Endocrinol Metab 2005; 90(5): 2804-9.
  87. Musso G, Gambino R, De MF, Cassader M, Rizzetto M, Durazzo M, et al. Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology 2003; 37(4): 909-16.
  88. Toshimitsu K, Matsuura B, Ohkubo I, Niiya T, Furukawa S, Hiasa Y, et al. Dietary habits and nutrient intake in non-alcoholic steatohepatitis. Nutrition 2007; 23(1): 46-52.
  89. Machado MV, Ravasco P, Jesus L, Marques-Vidal P, Oliveira CR, Proenca T, et al. Blood oxidative stress markers in non-alcoholic steatohepatitis and how it correlates with diet. Scand J Gastroenterol 2008; 43(1): 95-102.
  90. Simopoulos AP. Dietary omega-3 fatty acid deficiency and high fructose intake in the development of metabolic syndrome, brain metabolic abnormalities, and non-alcoholic fatty liver disease. Nutrients 2013; 5(8): 2901-23.
  91. Sekiya M, Yahagi N, Matsuzaka T, Najima Y, Nakakuki M, Nagai R, et al. Polyunsaturated fatty acids ameliorate hepatic steatosis in obese mice by SREBP-1 suppression. Hepatology 2003; 38(6): 1529-39.
  92. Levy JR, Clore JN, Stevens W. Dietary n-3 polyunsaturated fatty acids decrease hepatic triglycerides in Fischer 344 rats. Hepatology 2004; 39(3): 608-16.
  93. Ibrahim A, Natrajan S, Ghafoorunissa R. Dietary trans-fatty acids alter adipocyte plasma membrane fatty acid composition and insulin sensitivity in rats. Metabolism 2005; 54(2): 240-6.
  94. 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(5): 1146-55.
  95. Medeiros F, Casanova MA, Fraulob JC, Trindade M. How can diet influence the risk of stroke? Int J Hypertens 2012; 2012: 763507.
  96. Hernandez R, Martinez-Lara E, Canuelo A, del Moral ML, Blanco S, Siles E, et al. Steatosis recovery after treatment with a balanced sunflower or olive oil-based diet: involvement of perisinusoidal stellate cells. World J Gastroenterol 2005; 11(47): 7480-5.
  97. Bedogni G, Bellentani S. Fatty liver: how frequent is it and why? Ann Hepatol 2004; 3(2): 63-5.
  98. Cortez-Pinto H, Jesus L, Barros H, Lopes C, Moura MC, Camilo ME. How different is the dietary pattern in non-alcoholic steatohepatitis patients? Clin Nutr 2006; 25(5): 816-23.
  99. Zelber-Sagi S, Nitzan-Kaluski D, Goldsmith R, Webb M, Blendis L, Halpern Z, et al. Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): a population based study. J Hepatol 2007; 47(5): 711-7.
  100. Yasutake K, Nakamuta M, Shima Y, Ohyama A, Masuda K, Haruta N, et al. Nutritional investigation of non-obese patients with non-alcoholic fatty liver disease: the significance of dietary cholesterol. Scand J Gastroenterol 2009; 44(4): 471-7.
  101. Brownell KD, Farley T, Willett WC, Popkin BM, Chaloupka FJ, Thompson JW, et al. The public health and economic benefits of taxing sugar-sweetened beverages. N Engl J Med 2009; 361(16): 1599-605.
  102. Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer MJ, Willett WC, et al. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA 2004; 292(8): 927-34.
  103. Malik VS, Popkin BM, Bray GA, Despres JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care 2010; 33(11): 2477-83.
  104. Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z, Djibre A, et al. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Can J Gastroenterol 2008; 22(10): 811-6.
  105. Ouyang X, Cirillo P, Sautin Y, McCall S, Bruchette JL, Diehl AM, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol 2008; 48(6): 993-9.
  106. Abid A, Taha O, Nseir W, Farah R, Grosovski M, Assy N. Soft drink consumption is associated with fatty liver disease independent of metabolic syndrome. J Hepatol 2009; 51(5): 918-24.
  107. Abdelmalek MF, Suzuki A, Guy C, Unalp-Arida A, Colvin R, Johnson RJ, et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. Hepatology 2010; 51(6): 1961-71.
  108. Yesil A, Yilmaz Y. Review article: coffee consumption, the metabolic syndrome and non-alcoholic fatty liver disease. Aliment Pharmacol Ther 2013; 38(9): 1038-44.
  109. Pereira MA, Kartashov AI, Ebbeling CB, Van HL, Slattery ML, Jacobs DR, Jr., et al. Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet 2005; 365(9453): 36-42.
  110. Tetri LH, Basaranoglu M, Brunt EM, Yerian LM, Neuschwander-Tetri BA. Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent. Am J Physiol Gastrointest Liver Physiol 2008; 295(5): G987-G995.
  111. Marchesini G, Ridolfi V, Nepoti V. Hepatotoxicity of fast food? Gut 2008; 57(5): 568-70.