Novoe v profilaktike sakharnogo diabeta tipa 2


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Abstract

Учитывая, что СД типа 2 в настоящее время является неизлечимым заболеванием и тяжелым экономическим бременем для любого государства и семьи, причиной ранней инвалидизации людей трудоспособного возраста и высокой летальности, крайне актуальным становится изыскание путей профилактики или отсрочки его развития. За последнее десятилетие были предприняты несколько многоцентровых рандомизированных плацебо-контролируемых исследований, в которых наряду со стандартным или интенсивным изменением образа жизни использовали и лекарственные средства (акарбоза, метформин, орлистат). Продолжаются исследования и с другими препаратами. Росиглитазон в дозе 8 мг применен в исследовании DREAM (Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication) и показал высокую эффективность в профилактике СД типа 2. По сравнению с группой плацебо в группе росиглитазона снижение риска перехода НТГ в СД типа 2 составило 62%. Росиглитазон – безопасное и эффективное лекарственное средство не только для длительного применения у пациентов с СД типа 2, но и с НТГ с целью предупреждения или отсрочки развития СД типа 2.

About the authors

N. A Petunina

Московская медицинская академия им. И.М. Сеченова

Кафедра эндокринологии и диабетологии ФППО

References

  1. Ожирение. Под ред. И.И. Дедова, Г.А. Мельниченко, М.: МИА, 2004.
  2. Мкртумян А.М. Профилактика сахарного диабета типа 2 – не миф, а реальность. Consilium Medicum 2004; 6 (9).
  3. Boden G, Chen X. Effects of fat on glucose uptake and utilization in patients with non - insulin - dependent diabetes. J Clin Investigat 1995; 96: 1261–8.
  4. Dandona P, Aljada A, Bandyopadhyay A. Inflammation: the link between insulin resistance, obesity and diabetes. Trends Immunol 2004; 25: 4–7.
  5. Boden G, Shulman G.I. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and b - cell dysfunction. Eur J Clin Investigat 2002; 32 (Suppl. 3): 14–23.
  6. World Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications. Part I: Diagnosis and classification of diabetes mellitus. Geneva, WHO Department of Noncommunicable Disease Surveillance, 1999.
  7. Yki-Jarvinen H. Glucose toxicity. Endocrine Rev 1992; 13: 415–31.
  8. Lee Y, Hirose H, Ohneda M et al. Beta - cell lipotoxicity in the pathogenesis of non - insulin - dependent diabetes mellitus of obese rats: impairment in adipocyte - beta - cell relationships. Proceed Nat Acad Scien USA 1994; 91: 10878–82.
  9. Zhou Y.P, Grill V. Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans. J Clin Endocrinol Metabol 1995; 80: 1584–90.
  10. Shimabukuro M, Zhou Y.T, Levi M et al. Fatty acid - induced beta cell apoptosis: a link between obesity and diabetes. Proceed Nat Acad Scien USA 1998; 95: 2498–502.
  11. Bagust A, Beale S. Deteriorating beta - cell function in type 2 diabetes: a long - term model. Quarterly J Med 2003; 96: 281–8.
  12. UK Prospective Diabetes Study (UKPDS) Group. UK prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. Diabetes 1995; 44: 1249–58.
  13. Groop L.C. Insulin resistance: The fundamental trigger of type 2 diabetes. Diab Obes Metabol 1999; 1 (Suppl. 1): S1–S7.
  14. Del Prato S, Wishner W.J, Gromada J et al. Beta - cell mass plasticity in type 2 diabetes. Diab Obes Metab 2004; 6: 319–31.
  15. Weir G.C, Bonner-Weir S. Five stages of evolving beta - cell dysfunction during progression to diabetes. Diabetes 2004; 53 (Suppl. 3): S16–21.
  16. Butler A.E, Janson J, Bonner-Weir S et al. Beta - cell deficit and increased beta - cell apoptosis in humans with type 2 diabetes. Diabetes 2003; 52: 102–10.
  17. Bonora E, Targher G, Alberiche M et al. Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabet Care 2000; 23: 57–63.
  18. Buchanan T.A, Xiang A.H, Peters R.K et al. Preservation of pancreatic beta - cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high - risk hispanic women. Diabetes 2002; 51: 2796–803.
  19. Durbin R.J. Thiazolidinedione therapy in the prevention/delay of type 2 diabetes in patients with impaired glucose tolerance and insulin resistance. Diabet Obes Metab 2004; 6: 280–5.
  20. Knowler W.C, Hamman R.F, Edelstein S.L, et al. Prevention of type 2 diabetes with troglitazone in the diabetes prevention program. Diabetes 2005; 54: 1150–6.
  21. Fonseca V, Foyt H.L, Shen K et al. Long - term effects of troglitazone: open - label extension studies in type 2 diabetic patients. Diabet Care 2000; 23: 354–9.
  22. Einhorn D, Rendell M, Rosenzweig J et al. Pioglitazone hydrochloride in combination with metformin in the treatment of type 2 diabetes mellitus: a randomized, placebo - controlled study. The Pioglitazone 027 Study Group. Clin Therapeut 2000; 22: 1395–409.
  23. St John Sutton M, Rendell M, Dandona P et al. A comparison of the effects of rosiglitazone and glyburide on cardiovascular function and glycemic control in patients with type 2 diabetes mellitus. Diabet Care 2002; 25: 2058–64.
  24. Miyazaki Y, Mahankali A, Matsuda M et al. Improved glycemic control and enhanced insulin sensitivity in type 2 diabetic subjects treated with pioglitazone. Diabet Care 2001; 24: 710–9.
  25. Leiter L. b - cell preservation: a potential role for thiazolidinediones to improve clinical care in type 2 diabetes. Diab Med 2005; 22: 963–72.
  26. Juhl C.B, Hollingdal M, Porksen N et al. Influence of rosiglitazone treatment on beta - cell function in type 2 diabetes: evidence of an increased ability of glucose to entrain high - frequency insulin pulsatility. J Clin Endocrinol Metabol 2003; 88: 3794–800.
  27. Lupi R, Del Guerra S, Marselli L et al. Rosiglitazone prevents the impairment of human islet function induced by fatty acids: evidence for a role of PPARgamma2 in the modulation of insulin secretion. Am J Physiol Endocrinol Metab 2004; 286: E560–7.
  28. Smith S.A, Porter L.E, Biswas N et al. Rosiglitazone, but not glyburide, reduces circulating proinsulin and the proinsulin:insulin ratio in type 2 diabetes. Journal of Clinical Endocrinology and Metabolism 2004; 89: 6048–53.
  29. Gerstein H.C, Yusuf S, Holman R et al. Rationale, design and recruitment characteristics of a large, simple international trial of diabetes prevention: the DREAM trial. Diabetologia 2004; 47: 1519–27.
  30. Viberti G, Kahn S.E, Greene D.A et al. A Diabetes Outcome Progression Trial (ADOPT): An international multicenter study of the comparative efficacy of rosiglitazone, glyburide, and metformin in recently diagnosed type 2 diabetes. Diabet Care 2002; 25: 1737–43.
  31. Walter H, Lubben G. Potential role of oral thiazolidinedione therapy in preserving beta - cell function in type 2 diabetes mellitus. Drugs 2005; 65: 1–13.
  32. Gerstein H.C, Yusuf S, Holman R.R et al. Design and baseline characteristics of the DREAM (Diabetes REduction Assessment with ramipril and rosiglitazone Medication) trial. Diabetes 2004; 53 Suppl. 2: A483.

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