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Type 2 diabetes mellitus as a subclinical inflammation


Authors: Jan Škrha
Authors‘ workplace: Univerzita Karlova v Praze, 1. lékařská fakulta, III. interní klinika VFN
Published in: Čas. Lék. čes. 2010; 149: 277-281
Category: Review Article

Overview

Type 2 diabetes mellitus develops as a combination of genetic background and external factors. The disease development is caused by increased oxidative stress under various metabolic factors and in parallel by complex inflammatory reaction without clinical signs. The resulting subclinical inflammation is a consequence of defensive anti-inflammatory reactions. Such Type 2 diabetes conception brings various possibilities in the treatment and prevention.

Key words:
type 2 diabetes, oxidative stress, inflammation, anti-inflammatory mechanisms.


Sources

1. Kolb H, Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation. Diabetologia 2010; 53: 10–20.

2. Škrha J. Biochemie a patofyziologie. In: Diabetologie, eds. J. Škrha a spol. Praha: Galén 2009; 33–75.

3. Kintscher U, Hartge M, Hess K. et al. T-lymphocyte infiltration in visceral adipose tissue: a primary event in adipose tissue inflammation and the development of obesity-mediated insulin resistance. Arterioscl Thromb Vasc Biol 2008; 28: 1304–1310.

4. Hamdy O, Porramatikul S, Al Ozairi E. Metabolic obesity: the paradox between visceral and subcutaneous fat. Curr Diabetes Rev 2006; 2: 367–373.

5. Aljada A, Mohanty P, Ghanim H, et al. Increase in intranuclear nuclear factor kappa B and decrease in inhibitor kappaB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Am J Clin Nutr 2004; 79: 682–690.

6. Esposito K, Nappo F, Giugliano F, 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: 1135–1140.

7. Tripathy D, Mohanty P, Dhindsa S, et al. Elevation of free fatty acids induces inflammation and impairs vascular reactivity in healthy subjects. Diabetes 2003; 52: 2882–2887.

8. Blackburn P, Despres JP, Lamarche B, et al. Postprandial variations of plasma inflammatory markers in abdominally obese men. Obesity 2006; 14: 1747–1754.

9. Nappo F, Esposito K, Cioffi M, 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: 1145–1150.

10. Patel C, Ghanim H, Ravishankar S, et al. Prolonged reactive oxygen species generation and nuclear factor-kappaB activation after a high-fat, high-carbohydrate meal in the obese. J Clin Endocrinol Metab 2007; 92: 4476–4479.

11. Cani PD, Neyrinck AM, Fava F, et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxemia. Diabetologia 2007; 50: 2374–2383.

12. Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. TLR4 links innate imunity and fatty acid-induced insulin resistance. J Clin Invest 2006; 116: 3015–3025.

13. Milanski M, Degasperi G, Coope A, 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: 359–370.

14. Poggi M, Bastelica D, Gual P, et al. C3H/HeJ mice carrying a toll-like receptor 4 mutation are protected against the development of insulin resistance in white adipose tissue in response to a high-fat diet. Diabetologia 2007; 50: 1267–1276.

15. Cai D, Yuan M, Frantz DF, et al. Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF‑kappaB. Nat Med 2005; 11: 183–190.

16. Aarnes M, Schonberg S, Grill V. Fatty acids potentiate interleukin-1 beta toxicity in the beta-cell line INS-1E. Biochem Biophys Res Commun 2002; 296: 189–193.

17. Kim EK, Kwon KB, Koo BS, et al. Activation of peroxisome proliferator-activated receptor gamma protects pancreatic beta-cells from cytokine-induced cytotoxicity via NF kappaB pathway. Int J Biochem Cell Biol 2007; 39: 1260–1275.

18. Grunnet LG, Aikin R, Tonnesen MF, et al. Proinflammatory cytokines activate the intrinsic apoptotic pathway in the beta cells. Diabetes 2009; 58: 1807–1815.

19. Maedler K, Spinas GA, Dyntar D, Moritz W, Kaiser N, Donath MY. Distinct effects of saturated and monounsaturated fatty acids on beta-cell turnover and function. Diabetes 2001; 50: 69–76.

20. McGarry JD. Dysregulation of fatty acid metabolism in the etiology of type 2 diabetes. Diabetes 2002; 51: 7–18.

21. Haubner F, Lehle K, Munzel D, Schmid C, Birnbaum DE, Preuner JG. Hyperglycemia increases the levels of vascular cellular adhesion molecule-1 and monocyte-chemoatractant-protein-1 in the diabetic endothelial cell. Biochem. Biophys Res Commun 2007; 360: 560–565.

22. Dasu MR, Devaraj S, Jialal I. High glucose induces IL-1beta expression in human monocytes: mechanistic insights. Am J Physiol Endocrinol Metab 2007; 293: E337–E346.

23. Devaraj S, Venugopal SK, Singh U, Jialal I. Hyperglycemia induces monocytic release of interleukin-6 via induction of protein kinase C-α and ß. Diabetes 2005; 54: 85–91.

24. Piconi I, Quagliaro L, Da Ros R, et al. Intermittent high glucose enhances ICAM-1, VCAM-1, E-selectin and interleukin-6 expression in human umbilical endothelial cells in culture: the role of poly(ADP-ribose) polymerase. J Thromb Haemost 2004; 2: 1453–1459.

25. Esposito K, Marfella R, Ciotola M, et al. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA 2004; 292: 1440–1446.

26. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation 2002; 106: 2067–2072.

27. Kempf K, Rose B, Herder C, et al. The metabolic syndrome sensitizes leukocytes for glucose-induced immune gene expression. J Mol Med 2007; 85: 389–396.

28. Maedler K, Sergeev P, Ris F, et al. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest 2002; 110: 851–860.

29. Boni-Schnetzler M, Thorne J, Parnaud G, et al. Increased interleukin (IL)-1beta messenger ribonucleic acid expression in beta-cells of individuals with type 2 diabetes and regulation of IL-1beta in human islets by glucose and autostimulation. J Clin Endocrinol Metab 2008; 93: 4065–4074.

30. Herder C, Peltonen M, Koenig W, et al. Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study. Diabetologia 2009; 52: 433–442.

31. North CJ, Venter CS, Jerling JC. The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease. Eur J Clin Nutr 2009; 63: 921–933.

32. Mathur N, Pedersen BK. Exercise as a mean to control low-grade systemic inflammation. Mediators Inflamm 2008: 109502. dot:10.1155/2008/109502

33. Silva LA, Silveria PC, Pinho CA, Tuon T, Dal Pizzol F, Pinho RA. N-acetylcystein supplementation and oxidative damage and inflammatory response after eccentric exercise. Int J Sport Nutr Exerc Metab 2008; 18: 379–388.

34. Knol MJ, Twisk JW, Beekman AT, Heine RJ, Snoek FJ, Pouwer F. Depression as a risk factor for the onset of type 2 diabetes mellitus. A meta-analysis. Diabetologia 2006; 49: 837–845.

35. Tasali E, Leproult R, Spiegel K. Reduced sleep duration or duality: relationships with insulin resistance and type 2 diabetes. Prog Cardiovasc Dis 2009; 51: 381–391.

36. Meier-Ewert HK, Ridker PM, Rifai N, et al. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol 2004; 43: 678–683.

37. Irwin MR, Wang M, Ribeiro D, et al. Sleep loss activates cellular inflammatory signaling. Biol Psychiatry 2008; 64: 538–540.

38. Howren MB, Lamkin DM, Suls J. Associations of depression with C-reactive protein, IL-1, and IL-6: a meta-analysis. Psychosom Med 2009; 71: 171–186.

39. Tousoulis D, Drolias A, Antoniades C, et al. Antidepressive treatment as a modulator of inflammatory process in patients with heart failure: effects on proinflammatory cytokines and acute phase protein levels. Int J Cardiol 2009; 134: 238–243.

40. Maraldi C, Volpato S, Penninx BW, et al. Diabetes mellitus, glycemic control, and incident depressive symptoms among 70- to 79-year-old persons: the health, aging, and body composition study. Arch Intern Med 2007; 167: 1137–1144.

41. Pulkki-Raback L, Elovainio M, Kivimaki M, et al. Depressive symptoms and the metabolic syndrome in childhood and adulthood: a prospective cohort study. Health Psychol 2009; 28: 108–116.

42. Larsen CM, Faulenbach M, Vaag A, et al. Interleukin-1-receptor antagonist in type 2 diabetes mellitus. N Engl J Med 2007; 356: 1517–1526.

43. Berchtold LA, Larsen CM, Vaag A, et al. IL-1 receptor antagonism and muscle gene expression in patients with type 2 diabetes. Eur Cytokine Netw 2009; 20: 81–87.

44. Larsen CM, Faulenbach M, Vaag A, Ehses JA, Donath MY, Mandrup-Poulsen T. Sustained effects of interleukin-1-receptor antagonist treatment in type 2 diabetes mellitus. Diabetes Care 2009; 32: 1663–1668.

45. Koska J, Ortega E, Bunt JC, et al. The effect of salsalate on insulin action and glucose tolerance in obese non-diabetic patients: results of a randomised double-blind placebo controlled study. Diabetologia 2009; 52: 385–393.

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