Review
BibTex RIS Cite

Metabolik Sendrom Tedavisinde Bağırsak Mikrobiyotasının Probiyotikler ve Özelinde Saccharomyces Boulardii ile Modülasyonu

Year 2017, , 131 - 140, 07.03.2017
https://doi.org/10.21673/anadoluklin.260702

Abstract

Metabolik sendrom insan metabolizmasındaki dengenin bozulmasını ifade eden glukoz intoleransı veya diyabetes mellitus, abdominal obezite, dislipidemi, hipertansiyon, kardiyovasküler anormalliklerin bir arada görüldüğü hastalıklar kümesidir. Barındırdığı riskli hastalıklardan dolayı da mortalite ve morbiditesi artmaktadır. Türkiye’de ve dünyada metabolik sendrom prevelansı epidemik seviyelere ulaşmak üzere ve ülkelerin ekonomisine ağır yükler getirmektedir. Metabolik sendrom tedavisinde başlıca hedef kalp hastalıkları riskini azaltmak ve hastalığı kontrol altında tutmaktır bunun içinde ilaç tedavisi ve son yıllarda obezite özelinde cerrahi tedaviler uygulanmaktadır. Ancak ilaç tedavileri hasta yaşamında ciddi ve kalıcı değişimler yapmadıkça bu hastalık grubuna kesin çözüm getirmekten çok uzaktır. Cerrahi tedaviler için ise kesin yargılarda bulunmak henüz çok erkendir. Son zamanlarda insan mikrobiyatası üzerine yapılan bilimsel çalışmalar bağırsak mikrobiyatasında ki homeostatik dengenin bozulması nedeniyle subklinik ve kronik bir inflamasyonun oluştuğu ve bununda glukoz metabolizmasının bozulmasında rolü olduğu gösterilmiştir. Bu nedenle bağırsak mikrobiyotasını probiyotikler kullanarak modüle edip metabolik sendrom hastalarının tedavisinde kullanmak etkili ve ekonomik bir çözüm fırsatı olabilir. Yeni çıkan bir çalışmada Everard ve arkadaşları (98), Tip 2 diyabetes mellitusu olan farelere verilen Saccharomyces boulardii diyabetin klinik belirteçlerini geriletmiş ve metabolik sendromlu hastaların tedavisinde kullanılabileceğinin ön verilerini göstermiştir.


 

 

 

 

 

 

 


References

  • 1. Kozan O, Oguz A, Abaci A, et al. Prevalence of the metabolic syndrome among Turkish adults. Eur J Clin Nutr. 2007; 61(4):548-53.
  • 2. Onat A, Ceyhan K, Basar O., Erer B, Toprak S, Sansoy V. Metabolic syndrome: major impact on coronary risk in a population with low cholesterol levels--a prospective and cross-sectional evaluation. Atherosclerosis. 2002;165:285-92.
  • 3. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from theThird National Health and Nutrition Examination Survey. JAMA. 2002; 287:356–359.
  • 4. DeFronzo R.A, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidaemia, and atherosclerotic cardiovascular disease. Diabetes Care. 1991; 14:173-194.
  • 5. Isomaa B, Almgren P, Tuomi T, Forsén B, Lahti K, Nissén M, Taskinen MR, Groop L. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001;24(4):683-9.
  • 6. Ford ES. Risks for all-cause mortality, cardiovasc ular disease, and diabetes associated with the metabolic syndrome: a summary of the evidence. Diabetes Care. 2005; 28(7):1769-78.
  • 7. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988; 37(12):1595-1607.
  • 8. Kaplan NM. The deadly quartet. Upper-body obesity, glucose intolerance, hyper- triglyceridemia and hypertension. Arch Intern Med. 1989; 149:1514-1520.
  • 9. Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield S.B. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994. Arch Intern Med. 2003; 24;163(4):427-36.
  • 10. Balkau B, Charles MA.Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR). Diabet Med. 1999; 16(5):442-3.
  • 11. Balkau B, Charles MA, Drivsholm T, Borch-Johnsen K, Wareham N, Yudkin JS, et al. European Group for the Study of Insulin Resistance (EGIR). Frequency of the WHO metabolic syndrome in European cohorts, and an alternative definition of an insulin resistance syndrome. Diabetes Metabolism. 2002; 28(5):364-76.
  • 12. Turkendokrin.org [Internet]. Ankara; Metabolik Sedndrom Kılavuzu.2009. http://www.turkendokrin.org/files/pdf/metabolik_sendrom.pdf. 10.Temmuz.2016.
  • 13. Lorenzo C, Williams K, Hunt KJ, Haffner SM. The National Cholesterol Education Program - Adult Treatment Panel III, International Diabetes Federation, and World Health Organization definitions of the metabolic syndrome as predictors of incident cardiovascular disease and diabetes. Diabetes Care. 2007; 30(1):8-13.
  • 14. Lautt WW. Macedo MP, Sadri P, Legare DJ, Reid MA, Guarino MP. Pharmaceutical reversal of insulin resistance. Proc West Pharmacol Soc. 2004; 47:30-2.
  • 15. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shirit A, Fuchs Z. Hyperinsulinemia: a link between hypertension, obesity and glucose intolerance. J Clin Invest 1985; 75:807–817.
  • 16. Ahrén B. Pacini G. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. 2005; 7(1):2-8.
  • 17. Satman I. Turkendokrin.org [Internet]. Ankara; TURDEP Çalışma Grubu. 2011. http://www.turkendokrin.org/files/file/TURDEP_II_2011.pdf. 10.Temmuz.2016.
  • 18. Chiasson JL, Rabasa-Lhoret R. Prevention of type 2 diabetes: insulin resistance and beta-cell function. Diabetes. 2004; 53(3):34-8.
  • 19. Turkendokrin.org [Internet]. Ankara; Diabetes Mellitus ve Komplikasyonlarının Tanı, Tedavi ve İzlem Klavuzu. 2016.http://www.turkendokrin.org/files/file/DIYABET_TTK_web.pdf. 10.Temmuz.2016.
  • 20. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care. 2004; 27:1047–1053
  • 21. Hanson RL, Imperatore G, Bennett PH, Knowler WC. "Components of the "metabolic syndrome" and incidence of type 2 diabetes." Diabetes.2002; 51(10):3120-7.
  • 22. Kahn CR. Insulin action, diabetogenes, and the cause of type II diabetes. Diabetes. 1994; 43(8):1066-84.
  • 23. Cuspidi C, Meani S, Fusi V, et al. Metabolic syndrome and target organ damage in untreated essential hypertensives. J Hypertens. 2004; 22:1991–8.
  • 24. Schillaci G, Pirro M, Vaudo G, et al.. “Prognostic value of the metabolic syndrome in essential hypertension. J Am Coll Cardiol. 2004; 43:1817–22
  • 25. DeFronzo, R. A., 1981. The effect of insulin on renal sodium metabolism: a review with clinical implications.” Diabetologia. 21, 165- 171
  • 26. Leoncını G, Ratto E, Vıazzı F, Vaccaro V, Parodı D, Parodı A, et al. Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients. Journal of Internal Medicine. 2005; 257:454–460
  • 27. Lindsay RS, Howard BV. Cardiovascular risk associated with the metabolic syndrome. Curr Diab Rep. 2004; 4:63.
  • 28. Saely CH, Koch L, Schmid F, et al. Adult Treatment Panel III 2001 but not International Diabetes Federation 2005 criteria of the metabolic syndrome predict clinical cardiovascular events in subjects who underwent coronary angiography. Diabetes Care. 2006; 29(4):901-7.
  • 29. Wannamethee SG, Shaper AG, Lennon L, Morris RW. Metabolic syndrome vs Framingham Risk Score for prediction of coronary heart disease, stroke, and type 2 diabetes mellitus. Arch Intern Med. 2005; 165(22):2644-50.
  • 30. Preiss D, Sattar N. Non-alcoholic fatty liver disease: an overview of prevalence, diagnosis, pathogenesis and treatment considerations. Clin Sci (Lond). 2008; 115(5):141-50.
  • 31. Sattar N, Forrest E, Preiss D. Non-alcoholic fatty liver disease. BMJ. 2014; 29:349:g4596
  • 32. Langenberg C, Bergstrom J, Scheidt-Nave C, Pfeilschifter J, Barrett-Connor E. Cardiovascular death and the metabolic syndrome: role of adiposity-signaling hormones and inflammatory markers. Diabetes Care. 2006; 29(6):1363-9
  • 33. Saydah SH, Pavkov ME, Zhang C, et al. Albuminuria prevalence in first morning void compared with previous random urine from adults in the National Health and Nutrition Examination Survey. Clin Chem. 2013; 59:675 –68.
  • 34. Prasad GV. Metabolic syndrome and chronic kidney disease: Current status and future directions. World J Nephro. 2014; 3(4):210-9
  • 35. Pyorala M, Miettinen H, Halonen P, Laakso M, Pyorala K. Insulin resistance syndrome predicts the risk of coronary heart disease and stroke in healthy middle-aged men: the 22-year follow-up results of the Helsinki Policemen Study. Arterioscler Thromb Vasc Biol. 2000; 20:538–544
  • 36. Juhan-Vague I, Alessi MC. PAI-1, obesity, insulin resistance and risk of cardiovascular events. Thromb Haemost. 1997; 78:656–660.
  • 37. Imperatore G, Riccardi G, Iovine C, Rivellese AA, Vaccaro O. Plasma fibrinogen: a new factor of the metabolic syndrome: a population based study. Diabetes Care. 1998; 21:649–654.
  • 38. Chavez-Tapia NC, Mendez-Sanchez N, Uribe M. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med. 2006. 144:379.
  • 39. 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;143:722–728.
  • 40. Festi D, Schiumerini R, Marzi L, Di Biase AR, Mandolesi D, Montrone L, et al.Review article: the diagnosis of non-alcoholic fatty liver disease - availability and accuracy of non-invasive methods. Aliment Pharmacol Ther. 2013; 37(4):392-400.
  • 41. Williams CD, Stengel J, Asike MI, et al. Prevalence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among a largely middle-aged population utilizing ultrasound and liver biopsy: a prospective study. Gastroenterology, 2011; 140:124–31
  • 42. Levene AP, Goldin RD. The epidemiology, pathogenesis and histopathology of fatty liver disease. Histopathology. 2012; 61(2):141-52.
  • 43. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology. 2006;43(2):99-112.
  • 44. Tiikkainen M, Bergholm R, Vehkavaara S, Rissanen A, Hakkinen AM, Tamminen M, Teramo K, YkiJarvinen H. Effects of identical weight loss on body composition and features of insulin resistance in obese women with high and low liver fat content. Diabetes. 2003;52:701–707.
  • 45. Kotronen A, Juurinen L, Hakkarainen A, Westerbacka J, Corner A, Bergholm R, et al. Liver fat is increased in type 2 diabetic patients and underestimated by serum alanine aminotransferase compared with equally obese nondiabetic subjects. Diabetes Care. 2008; 31:165–169.
  • 46. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW.C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue. Arterioscler Thromb Vasc Biol. 1999; 19(4):972-8
  • 47. Festa A, D'Agostino RJr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000; 102(1):42-7
  • 48. Timpson NJ, Lawlor DA, Harbord RM, Gaunt TR, Day IN, Palmer LJ, et al. C-reactive protein and its role in metabolic syndrome: mendelian randomisation study. Lancet. 2005; 366(9501):1954-9
  • 49. Pasquali R, Gambineri A, Anconetani B, et al. The natural history of the metabolic syndrome in young women with the polycystic ovary syndrome and the effect of long-term oestrogen-progestagen treatment. Clin Endocrinol (Oxf). 1999;50:517.
  • 50. Pasquali R, Gambineri A, Pagotto U. The impact of obesity on reproduction in women with polycystic ovary syndrome. BJOG. 2006;113(10):1148-59.
  • 51. Azziz JR, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens KC, et al. Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab. 2004; 89:453–62.
  • 52. Kaneto H, Katakami N, Matsuhisa M, Matsuoka TA. Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis. Mediators Inflamm. 2010; 2010:453892.
  • 53. Rao MS, Reddy JK. Peroxisomal beta-oxidation and steatohepatitis. Semin Liver Dis. 2001; 21(1):43-55.
  • 54. Reddy JK. Nonalcoholic steatosis and steatohepatitis. III.Peroxisomal beta-oxidation, PPAR alpha, and steatohepatitis. Am. J. Physiol. Gastrointest. Liver Physiol. 2001; 281:1333–1339.
  • 55. Sanyal AJ, Campbell-Sargent C, Mirshahi F, et al. Nonalcoholicsteatohepatitis: association of insulin resistance and mitochondrial abnormalities. Gastroenterology. 2001; 120:1183–1192
  • 56. George J, Pera N, Phung N, Leclercq I, Yun Hou J, Farrell G. Lipid peroxidation, stellate cell activation and hepatic fibrogenesis in a rat model of chronic steatohepatitis. J. Hepatol. 2003; 39:756–764.
  • 57. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insülin resistance. Diabetes. 2007; 56:1761–72.
  • 58. Neish AS. Microbes in gastrointestinal health and disease. Gastroenterology. 2009; 136(1):65–80
  • 59. Ma YY, Li L, Yu CH, Shen Z, Chen LH, Li YM. Effects of probiotics on nonalcoholic fatty liver disease: a meta-analysis. World J Gastroenterol. 2013; 19(40):6911-8
  • 60. Iacono A, Raso GM, Canani RB, Calignano A, Meli R. Probiotics as emerging therapeutic strategy to treat NAFLD: focus on molecular and biochemicalmechanisms. J Nutr Biochem. 2011;22(8):699-711.
  • 61. Backhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host–bacterial mutualism in the human intestine. Science, 2005; 307(5717):1915–20.
  • 62. Eckburg PB, Bik EM, Bernstein CN, Purdom E, Dethlefsen L, Sargent M, et al. Diversity of the human intestinal microbial flora. Science. 2005; 308(5728):1635–8.
  • 63. Backhed F, Ding H, Wang T, et al. The gutmicrobiota as an environmental factor that regulates fat storage. Proceedings of the National Academy of Sciences of the United States of Americ. 2004; 101(44):15718–15723.
  • 64. Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009; 9:13-23
  • 65. Everard A, Cani PD. Diabetes, obesity and gut microbiota. Best Pract Res Clin Gastroenterol. 2013;27(1):73-83.
  • 66. Shen J, Obin MS, Zhao L. The gut microbiota, obesity and insulin resistance. Mol Aspects Med. 2013; 34:39–5.
  • 67. Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008; 57:1470–81.
  • 68. Miele L, Valenza V, La Torre G, Montalto M, Cammarota G, Ricci R, et al. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Hepatology. 2009; 49(6):1877-87
  • 69. Brun P, Castagliuolo I, Buda. A, Pinzani M, Palù G, Martines DV. Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. American Journal of Physiology. 2007; 292(2):518-25.
  • 70. Amar J, Chabo C, Waget A, Klopp P, Vachoux C, Bermudez-Humaran LG, et al. Intestinal mucosal adherence and translocation of commensal bacteria at the early onset of type 2 diabetes: molecular mechanisms and probiotic treatment. EMBO Mol Med. 2011; 3:559–72.
  • 71. Vieira AT, Teixeira MM, Martins FS. The role of probiotics and prebiotics in inducing gut immunity. Front Immunol. 2013; 12(4):445-57.
  • 72. Larsen N, Vogensen FK, Van den Berg FWJ, et al. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One. 2010; 5(2) Article ID e9085
  • 73 .Santacruz A, Marcos A, Wärnberg J, Martí A, Martin-Matillas M, Campoy C, et al. Interplay between weight loss and gut microbiota composition in overweight adolescents. Obesity (Silver Spring). 2009; 17(10):1906-15.
  • 74. Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci USA. 2005; 102:11070–5.
  • 75. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesityassociated gut microbiome with increased capacity for energy harvest. Nature. 2006; 444:1027–31.
  • 76. Vrieze A, Van Nood E, Holleman F, Salojarvi J, Kootte RS, Bartelsman JF, et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology. 2012;143: 913–917.
  • 77. Fanaro S, Chierici R, Guerrini P, Vigi V. Intestinal microflora in early infancy:composition and development.Acta Paediatr Suppl. 2003; 91(441):48–55.
  • 78. Lyte M. Probiotics function mechanistically as delivery vehicles for neuroactive compounds: Microbial endocrinology in the design and use of probiotics. Bioessays. 2011; 33:574–581.
  • 79. Madsen K, Cornish A, Soper P, McKaigney C, Jijon H,Yachimec C, et al. Probiotic bacteria enhance murine and human intestinal epithelial barrierfunction. Gastroenterology. 2001; 121:580-591
  • 80. Ulisse S, Gionchetti P, D‟Alo S, Russo FP, Pesce I, Ricci G, et al. Expression of cytokines, inducible nitric oxide synthase, and matrix metalloproteinases in pouchitis: effects of probiotic treatment. Am J Gastroenterol. 2001; 96:2691–9.
  • 81. Guarner F, Malagelada JR. Gut flora in health and disease. Lancet. 2003; 361:512-519.
  • 82. Mach T. Clinical usefulness of probiotics in inflammatory bowel diseases. J Physiol Pharmacol. 2006; 9:23–33.
  • 83. O’Hara AM, Shanahan F. Mechanisms of action of probiotics in intestinal diseases. ScientificWorld Journal. 2007; 7:31–46.
  • 84. Sakata T, Kojima T, Fujieda M, Takahashi M, Michibata T. Influences of probiotic bacteria on organic acid production by pig caecal bacteria in vitro. Proc Nutr Soc. 2003: 62(1):73–80.
  • 85. Attene-Ramos MS, Wagner ED, Gaskins HR, Plewa MJ. Hydrogen sulfide induces direct radicalassociated DNA damage. Mol Cancer Res. 2007; 5(5):455–9.
  • 86. Santacruz A, Marcos A, Warnberg J, et al. Interplay between weight loss and gut microbiota composition in overweight adolescents, Obesity. 2009; 17(10):1906–1915.
  • 87. Kimmey MB, Elmer GW, Surawicz CM, et al. Prevention of further recurrences of Clostridium difficile colitis with Saccharomyces boulardii. Dig Dis Sci. 1990; 35:897-901.
  • 88. Schneider SM, Girard-Pipau F, Filippi J, et al. Effects of Saccharomyces boulardii on fecal shortchain fatty acids and microflora in patients on long-term total enteral nutrition. World J Gastroenterol. 2005; 11:6165–6169.
  • 89. Graff S, Chaumeil JC, Boy P, Lai-Kuen R, Charrueau C. Influence of pH conditions on the viability of Saccharomyces boulardii yeast. J. Gen.Appl. Microbiol. 2008; 54:221–227.
  • 90. Blehaut H, Massot J, Elmer GW, et al. Disposition kinetics of Saccharomyces boulardii in man and rat. Biopharm Drug Dispos. 1989; 10(4):353-64.
  • 91. Pothoulakis C. Review article: anti-inflammatory mechanisms of action of Saccharomyces boulardii. Aliment Pharmacol Ther. 2009; 30(8):826-33
  • 92. Im E, Pothoulakis C. Recent advances in Saccharomyces boulardii research. Gastroenterol Clin Biol. 2010;34(1):S62-70.
  • 93. Stienstra R, Duval C, Muller M, Kersten S. PPARs, obesity, and inflammation. PPAR Res. 2007; 283(33):22620-7.
  • 94. Pallone F, Monteleone G. Mechanisms of tissue damage in inflammatory bowel disease. Curr Opin Gastroenterol. 2001; 17:307–12
  • 95. Naumann M. Nuclear factor-kappa B activation and innate immune response in microbial pathogen infection. Biochem Pharmacol. 2000: 60:1109–14.
  • 96. Sougioultzis S, Simeonidis S, Bhaskar KR, et al. Saccharomyces boulardii produces a soluble anti-inflammatory factor that inhibits NF-kappaB-mediated IL-8 gene expression. Biochem Biophys Res Commun. 2006; 343:69–76.

The modulation of gut microbiota with probiotics and especially with saccharomyces boulardii in treatment of metabolic syndrome

Year 2017, , 131 - 140, 07.03.2017
https://doi.org/10.21673/anadoluklin.260702

Abstract

Metabolic Syndrome shows up with the group of diseases that mean the impairment of human metabolism such as, glucose intolerance or diabetes mellitus, abdominal obesity, dislipidemi , hypertension, cardiovascular. Because of risky diseases that Metabolic syndrome consists, morality and mordibity increase. In Turkey and also in the world the prevalence of metabolic syndrome almost reaches the epidemic level and it brings heavy burden to countries’ economies. The main goal of metabolic syndrome treatment is to minimize risks of heart diseases and to control the disease. To reach that goal medication and surgical treatment that are specified in obesity, have been applied. However it is too difficult to make an absolute solution unless the medication makes some serious and permanent changes in patient’s life. It is also too early to say that surgical treatment have absolute results. The last researches on human microbiota have shown that because of the impairment of the homeostatic balance in intestinal microbiota, subclinical and chronic inflammation occurs, and they also have shown that the inflammation has a role in the impairment of glucose metabolism. Therefore, to modulate the probiotics in the intestinal microbiota and use them for the treatment of metabolic syndrome can be an opportunity of an economic and an effective solution. In a new study, Everard and Everard’s friends(98) decrease the clinical indicators of Sacchromyces boulardii diabetes that has been given to mice that have Type2 diabetes mellitus and with that study, the preliminary data of using S. boulardii diabetes in the treatment of metabolic syndrome has been shown.


References

  • 1. Kozan O, Oguz A, Abaci A, et al. Prevalence of the metabolic syndrome among Turkish adults. Eur J Clin Nutr. 2007; 61(4):548-53.
  • 2. Onat A, Ceyhan K, Basar O., Erer B, Toprak S, Sansoy V. Metabolic syndrome: major impact on coronary risk in a population with low cholesterol levels--a prospective and cross-sectional evaluation. Atherosclerosis. 2002;165:285-92.
  • 3. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from theThird National Health and Nutrition Examination Survey. JAMA. 2002; 287:356–359.
  • 4. DeFronzo R.A, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidaemia, and atherosclerotic cardiovascular disease. Diabetes Care. 1991; 14:173-194.
  • 5. Isomaa B, Almgren P, Tuomi T, Forsén B, Lahti K, Nissén M, Taskinen MR, Groop L. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001;24(4):683-9.
  • 6. Ford ES. Risks for all-cause mortality, cardiovasc ular disease, and diabetes associated with the metabolic syndrome: a summary of the evidence. Diabetes Care. 2005; 28(7):1769-78.
  • 7. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988; 37(12):1595-1607.
  • 8. Kaplan NM. The deadly quartet. Upper-body obesity, glucose intolerance, hyper- triglyceridemia and hypertension. Arch Intern Med. 1989; 149:1514-1520.
  • 9. Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield S.B. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994. Arch Intern Med. 2003; 24;163(4):427-36.
  • 10. Balkau B, Charles MA.Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR). Diabet Med. 1999; 16(5):442-3.
  • 11. Balkau B, Charles MA, Drivsholm T, Borch-Johnsen K, Wareham N, Yudkin JS, et al. European Group for the Study of Insulin Resistance (EGIR). Frequency of the WHO metabolic syndrome in European cohorts, and an alternative definition of an insulin resistance syndrome. Diabetes Metabolism. 2002; 28(5):364-76.
  • 12. Turkendokrin.org [Internet]. Ankara; Metabolik Sedndrom Kılavuzu.2009. http://www.turkendokrin.org/files/pdf/metabolik_sendrom.pdf. 10.Temmuz.2016.
  • 13. Lorenzo C, Williams K, Hunt KJ, Haffner SM. The National Cholesterol Education Program - Adult Treatment Panel III, International Diabetes Federation, and World Health Organization definitions of the metabolic syndrome as predictors of incident cardiovascular disease and diabetes. Diabetes Care. 2007; 30(1):8-13.
  • 14. Lautt WW. Macedo MP, Sadri P, Legare DJ, Reid MA, Guarino MP. Pharmaceutical reversal of insulin resistance. Proc West Pharmacol Soc. 2004; 47:30-2.
  • 15. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shirit A, Fuchs Z. Hyperinsulinemia: a link between hypertension, obesity and glucose intolerance. J Clin Invest 1985; 75:807–817.
  • 16. Ahrén B. Pacini G. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. 2005; 7(1):2-8.
  • 17. Satman I. Turkendokrin.org [Internet]. Ankara; TURDEP Çalışma Grubu. 2011. http://www.turkendokrin.org/files/file/TURDEP_II_2011.pdf. 10.Temmuz.2016.
  • 18. Chiasson JL, Rabasa-Lhoret R. Prevention of type 2 diabetes: insulin resistance and beta-cell function. Diabetes. 2004; 53(3):34-8.
  • 19. Turkendokrin.org [Internet]. Ankara; Diabetes Mellitus ve Komplikasyonlarının Tanı, Tedavi ve İzlem Klavuzu. 2016.http://www.turkendokrin.org/files/file/DIYABET_TTK_web.pdf. 10.Temmuz.2016.
  • 20. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care. 2004; 27:1047–1053
  • 21. Hanson RL, Imperatore G, Bennett PH, Knowler WC. "Components of the "metabolic syndrome" and incidence of type 2 diabetes." Diabetes.2002; 51(10):3120-7.
  • 22. Kahn CR. Insulin action, diabetogenes, and the cause of type II diabetes. Diabetes. 1994; 43(8):1066-84.
  • 23. Cuspidi C, Meani S, Fusi V, et al. Metabolic syndrome and target organ damage in untreated essential hypertensives. J Hypertens. 2004; 22:1991–8.
  • 24. Schillaci G, Pirro M, Vaudo G, et al.. “Prognostic value of the metabolic syndrome in essential hypertension. J Am Coll Cardiol. 2004; 43:1817–22
  • 25. DeFronzo, R. A., 1981. The effect of insulin on renal sodium metabolism: a review with clinical implications.” Diabetologia. 21, 165- 171
  • 26. Leoncını G, Ratto E, Vıazzı F, Vaccaro V, Parodı D, Parodı A, et al. Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients. Journal of Internal Medicine. 2005; 257:454–460
  • 27. Lindsay RS, Howard BV. Cardiovascular risk associated with the metabolic syndrome. Curr Diab Rep. 2004; 4:63.
  • 28. Saely CH, Koch L, Schmid F, et al. Adult Treatment Panel III 2001 but not International Diabetes Federation 2005 criteria of the metabolic syndrome predict clinical cardiovascular events in subjects who underwent coronary angiography. Diabetes Care. 2006; 29(4):901-7.
  • 29. Wannamethee SG, Shaper AG, Lennon L, Morris RW. Metabolic syndrome vs Framingham Risk Score for prediction of coronary heart disease, stroke, and type 2 diabetes mellitus. Arch Intern Med. 2005; 165(22):2644-50.
  • 30. Preiss D, Sattar N. Non-alcoholic fatty liver disease: an overview of prevalence, diagnosis, pathogenesis and treatment considerations. Clin Sci (Lond). 2008; 115(5):141-50.
  • 31. Sattar N, Forrest E, Preiss D. Non-alcoholic fatty liver disease. BMJ. 2014; 29:349:g4596
  • 32. Langenberg C, Bergstrom J, Scheidt-Nave C, Pfeilschifter J, Barrett-Connor E. Cardiovascular death and the metabolic syndrome: role of adiposity-signaling hormones and inflammatory markers. Diabetes Care. 2006; 29(6):1363-9
  • 33. Saydah SH, Pavkov ME, Zhang C, et al. Albuminuria prevalence in first morning void compared with previous random urine from adults in the National Health and Nutrition Examination Survey. Clin Chem. 2013; 59:675 –68.
  • 34. Prasad GV. Metabolic syndrome and chronic kidney disease: Current status and future directions. World J Nephro. 2014; 3(4):210-9
  • 35. Pyorala M, Miettinen H, Halonen P, Laakso M, Pyorala K. Insulin resistance syndrome predicts the risk of coronary heart disease and stroke in healthy middle-aged men: the 22-year follow-up results of the Helsinki Policemen Study. Arterioscler Thromb Vasc Biol. 2000; 20:538–544
  • 36. Juhan-Vague I, Alessi MC. PAI-1, obesity, insulin resistance and risk of cardiovascular events. Thromb Haemost. 1997; 78:656–660.
  • 37. Imperatore G, Riccardi G, Iovine C, Rivellese AA, Vaccaro O. Plasma fibrinogen: a new factor of the metabolic syndrome: a population based study. Diabetes Care. 1998; 21:649–654.
  • 38. Chavez-Tapia NC, Mendez-Sanchez N, Uribe M. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med. 2006. 144:379.
  • 39. 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;143:722–728.
  • 40. Festi D, Schiumerini R, Marzi L, Di Biase AR, Mandolesi D, Montrone L, et al.Review article: the diagnosis of non-alcoholic fatty liver disease - availability and accuracy of non-invasive methods. Aliment Pharmacol Ther. 2013; 37(4):392-400.
  • 41. Williams CD, Stengel J, Asike MI, et al. Prevalence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among a largely middle-aged population utilizing ultrasound and liver biopsy: a prospective study. Gastroenterology, 2011; 140:124–31
  • 42. Levene AP, Goldin RD. The epidemiology, pathogenesis and histopathology of fatty liver disease. Histopathology. 2012; 61(2):141-52.
  • 43. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology. 2006;43(2):99-112.
  • 44. Tiikkainen M, Bergholm R, Vehkavaara S, Rissanen A, Hakkinen AM, Tamminen M, Teramo K, YkiJarvinen H. Effects of identical weight loss on body composition and features of insulin resistance in obese women with high and low liver fat content. Diabetes. 2003;52:701–707.
  • 45. Kotronen A, Juurinen L, Hakkarainen A, Westerbacka J, Corner A, Bergholm R, et al. Liver fat is increased in type 2 diabetic patients and underestimated by serum alanine aminotransferase compared with equally obese nondiabetic subjects. Diabetes Care. 2008; 31:165–169.
  • 46. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW.C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue. Arterioscler Thromb Vasc Biol. 1999; 19(4):972-8
  • 47. Festa A, D'Agostino RJr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000; 102(1):42-7
  • 48. Timpson NJ, Lawlor DA, Harbord RM, Gaunt TR, Day IN, Palmer LJ, et al. C-reactive protein and its role in metabolic syndrome: mendelian randomisation study. Lancet. 2005; 366(9501):1954-9
  • 49. Pasquali R, Gambineri A, Anconetani B, et al. The natural history of the metabolic syndrome in young women with the polycystic ovary syndrome and the effect of long-term oestrogen-progestagen treatment. Clin Endocrinol (Oxf). 1999;50:517.
  • 50. Pasquali R, Gambineri A, Pagotto U. The impact of obesity on reproduction in women with polycystic ovary syndrome. BJOG. 2006;113(10):1148-59.
  • 51. Azziz JR, Sanchez LA, Knochenhauer ES, Moran C, Lazenby J, Stephens KC, et al. Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab. 2004; 89:453–62.
  • 52. Kaneto H, Katakami N, Matsuhisa M, Matsuoka TA. Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis. Mediators Inflamm. 2010; 2010:453892.
  • 53. Rao MS, Reddy JK. Peroxisomal beta-oxidation and steatohepatitis. Semin Liver Dis. 2001; 21(1):43-55.
  • 54. Reddy JK. Nonalcoholic steatosis and steatohepatitis. III.Peroxisomal beta-oxidation, PPAR alpha, and steatohepatitis. Am. J. Physiol. Gastrointest. Liver Physiol. 2001; 281:1333–1339.
  • 55. Sanyal AJ, Campbell-Sargent C, Mirshahi F, et al. Nonalcoholicsteatohepatitis: association of insulin resistance and mitochondrial abnormalities. Gastroenterology. 2001; 120:1183–1192
  • 56. George J, Pera N, Phung N, Leclercq I, Yun Hou J, Farrell G. Lipid peroxidation, stellate cell activation and hepatic fibrogenesis in a rat model of chronic steatohepatitis. J. Hepatol. 2003; 39:756–764.
  • 57. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insülin resistance. Diabetes. 2007; 56:1761–72.
  • 58. Neish AS. Microbes in gastrointestinal health and disease. Gastroenterology. 2009; 136(1):65–80
  • 59. Ma YY, Li L, Yu CH, Shen Z, Chen LH, Li YM. Effects of probiotics on nonalcoholic fatty liver disease: a meta-analysis. World J Gastroenterol. 2013; 19(40):6911-8
  • 60. Iacono A, Raso GM, Canani RB, Calignano A, Meli R. Probiotics as emerging therapeutic strategy to treat NAFLD: focus on molecular and biochemicalmechanisms. J Nutr Biochem. 2011;22(8):699-711.
  • 61. Backhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host–bacterial mutualism in the human intestine. Science, 2005; 307(5717):1915–20.
  • 62. Eckburg PB, Bik EM, Bernstein CN, Purdom E, Dethlefsen L, Sargent M, et al. Diversity of the human intestinal microbial flora. Science. 2005; 308(5728):1635–8.
  • 63. Backhed F, Ding H, Wang T, et al. The gutmicrobiota as an environmental factor that regulates fat storage. Proceedings of the National Academy of Sciences of the United States of Americ. 2004; 101(44):15718–15723.
  • 64. Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol. 2009; 9:13-23
  • 65. Everard A, Cani PD. Diabetes, obesity and gut microbiota. Best Pract Res Clin Gastroenterol. 2013;27(1):73-83.
  • 66. Shen J, Obin MS, Zhao L. The gut microbiota, obesity and insulin resistance. Mol Aspects Med. 2013; 34:39–5.
  • 67. Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008; 57:1470–81.
  • 68. Miele L, Valenza V, La Torre G, Montalto M, Cammarota G, Ricci R, et al. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Hepatology. 2009; 49(6):1877-87
  • 69. Brun P, Castagliuolo I, Buda. A, Pinzani M, Palù G, Martines DV. Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. American Journal of Physiology. 2007; 292(2):518-25.
  • 70. Amar J, Chabo C, Waget A, Klopp P, Vachoux C, Bermudez-Humaran LG, et al. Intestinal mucosal adherence and translocation of commensal bacteria at the early onset of type 2 diabetes: molecular mechanisms and probiotic treatment. EMBO Mol Med. 2011; 3:559–72.
  • 71. Vieira AT, Teixeira MM, Martins FS. The role of probiotics and prebiotics in inducing gut immunity. Front Immunol. 2013; 12(4):445-57.
  • 72. Larsen N, Vogensen FK, Van den Berg FWJ, et al. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One. 2010; 5(2) Article ID e9085
  • 73 .Santacruz A, Marcos A, Wärnberg J, Martí A, Martin-Matillas M, Campoy C, et al. Interplay between weight loss and gut microbiota composition in overweight adolescents. Obesity (Silver Spring). 2009; 17(10):1906-15.
  • 74. Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci USA. 2005; 102:11070–5.
  • 75. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesityassociated gut microbiome with increased capacity for energy harvest. Nature. 2006; 444:1027–31.
  • 76. Vrieze A, Van Nood E, Holleman F, Salojarvi J, Kootte RS, Bartelsman JF, et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology. 2012;143: 913–917.
  • 77. Fanaro S, Chierici R, Guerrini P, Vigi V. Intestinal microflora in early infancy:composition and development.Acta Paediatr Suppl. 2003; 91(441):48–55.
  • 78. Lyte M. Probiotics function mechanistically as delivery vehicles for neuroactive compounds: Microbial endocrinology in the design and use of probiotics. Bioessays. 2011; 33:574–581.
  • 79. Madsen K, Cornish A, Soper P, McKaigney C, Jijon H,Yachimec C, et al. Probiotic bacteria enhance murine and human intestinal epithelial barrierfunction. Gastroenterology. 2001; 121:580-591
  • 80. Ulisse S, Gionchetti P, D‟Alo S, Russo FP, Pesce I, Ricci G, et al. Expression of cytokines, inducible nitric oxide synthase, and matrix metalloproteinases in pouchitis: effects of probiotic treatment. Am J Gastroenterol. 2001; 96:2691–9.
  • 81. Guarner F, Malagelada JR. Gut flora in health and disease. Lancet. 2003; 361:512-519.
  • 82. Mach T. Clinical usefulness of probiotics in inflammatory bowel diseases. J Physiol Pharmacol. 2006; 9:23–33.
  • 83. O’Hara AM, Shanahan F. Mechanisms of action of probiotics in intestinal diseases. ScientificWorld Journal. 2007; 7:31–46.
  • 84. Sakata T, Kojima T, Fujieda M, Takahashi M, Michibata T. Influences of probiotic bacteria on organic acid production by pig caecal bacteria in vitro. Proc Nutr Soc. 2003: 62(1):73–80.
  • 85. Attene-Ramos MS, Wagner ED, Gaskins HR, Plewa MJ. Hydrogen sulfide induces direct radicalassociated DNA damage. Mol Cancer Res. 2007; 5(5):455–9.
  • 86. Santacruz A, Marcos A, Warnberg J, et al. Interplay between weight loss and gut microbiota composition in overweight adolescents, Obesity. 2009; 17(10):1906–1915.
  • 87. Kimmey MB, Elmer GW, Surawicz CM, et al. Prevention of further recurrences of Clostridium difficile colitis with Saccharomyces boulardii. Dig Dis Sci. 1990; 35:897-901.
  • 88. Schneider SM, Girard-Pipau F, Filippi J, et al. Effects of Saccharomyces boulardii on fecal shortchain fatty acids and microflora in patients on long-term total enteral nutrition. World J Gastroenterol. 2005; 11:6165–6169.
  • 89. Graff S, Chaumeil JC, Boy P, Lai-Kuen R, Charrueau C. Influence of pH conditions on the viability of Saccharomyces boulardii yeast. J. Gen.Appl. Microbiol. 2008; 54:221–227.
  • 90. Blehaut H, Massot J, Elmer GW, et al. Disposition kinetics of Saccharomyces boulardii in man and rat. Biopharm Drug Dispos. 1989; 10(4):353-64.
  • 91. Pothoulakis C. Review article: anti-inflammatory mechanisms of action of Saccharomyces boulardii. Aliment Pharmacol Ther. 2009; 30(8):826-33
  • 92. Im E, Pothoulakis C. Recent advances in Saccharomyces boulardii research. Gastroenterol Clin Biol. 2010;34(1):S62-70.
  • 93. Stienstra R, Duval C, Muller M, Kersten S. PPARs, obesity, and inflammation. PPAR Res. 2007; 283(33):22620-7.
  • 94. Pallone F, Monteleone G. Mechanisms of tissue damage in inflammatory bowel disease. Curr Opin Gastroenterol. 2001; 17:307–12
  • 95. Naumann M. Nuclear factor-kappa B activation and innate immune response in microbial pathogen infection. Biochem Pharmacol. 2000: 60:1109–14.
  • 96. Sougioultzis S, Simeonidis S, Bhaskar KR, et al. Saccharomyces boulardii produces a soluble anti-inflammatory factor that inhibits NF-kappaB-mediated IL-8 gene expression. Biochem Biophys Res Commun. 2006; 343:69–76.
There are 96 citations in total.

Details

Journal Section REVİEW
Authors

İhsan Boyacı

Süleyman Yıldırım This is me

Publication Date March 7, 2017
Acceptance Date March 7, 2017
Published in Issue Year 2017

Cite

Vancouver Boyacı İ, Yıldırım S. The modulation of gut microbiota with probiotics and especially with saccharomyces boulardii in treatment of metabolic syndrome. Anadolu Klin. 2017;22(2):131-40.

13151 This Journal licensed under a CC BY-NC (Creative Commons Attribution-NonCommercial 4.0) International License.