medigraphic.com
SPANISH

Revista de Enfermedades no Transmisibles Finlay

ISSN 2221-2434 (Electronic)
  • Contents
  • View Archive
  • Information
    • General Information        
    • Directory
  • Publish
    • Instructions for authors        
  • medigraphic.com
    • Home
    • Journals index            
    • Register / Login
  • Mi perfil

2013, Number 4

<< Back Next >>

Finlay 2013; 3 (4)

Etiology and pathogenesis of diabetic microangiopathy. Biochemical and molecular considerations

León RML, González OLH, González OZA, de Armas GJO, Urquiza HA, Rodríguez CG
Full text How to cite this article

Language: Spanish
References: 34
Page: 241-254
PDF size: 195.03 Kb.


Key words:

diabetic angiopathies, diabetes complications, hyperglycemia, metabolism, oxidative stress.

ABSTRACT

Diabetes mellitus is a metabolic disease widely spread today, causing high costs to health and the global economy. Microangiopathy is one of its most significant late complications and the leading cause of disabling complications in advanced diabetes. This paper aimed at describing the etiology and pathogenesis of diabetic microangiopathy considering the current knowledge about the involved molecular events and their particular manifestation in diabetic nephropathy and retinopathy. It was concluded that the fundamental metabolic cause of diabetic microangiopathy is chronic hyperglycemia, which can modify intracellular metabolic pathways, as well as the protein structure and composition and increase the oxidative stress.


REFERENCES

  1. Organización Mundial de la Salud. Diabetes [Internet]. Ginebra: Organización Mundial de la Salud; 2013. [ cited 13 Abr 2013 ] Available from: http://www.who.int/mediacentre/factsheets/fs312 /es/index.html.

  2. Ministerio de Salud Pública. Anuario Estadístico de Salud 2011 [Internet]. La Habana: Dirección Nacional de Estadísticas; 2011. [ cited Sep 2012 ] Available from: http://www.sld.cu/sitios/dne.

  3. Ministerio de Salud Pública. Anuario Estadístico de Salud 2012 [Internet]. La Habana: Dirección Nacional de Estadísticas; 2012. [ cited Sep 2013 ] Available from: http://www.sld.cu/sitios/dne.

  4. Triana ME. La hiperglicemia y sus efectos tóxicos. Un concepto patogénico para la micro y macroangiopatía diabética. Rev Cubana Angiol y Cir Vasc. 2001 ; 2 (2): 131-41.

  5. Maitra AK, Abbas A. El sistema endocrino. In: Robins y Cotran. Patología Estructural y Funcional. 7ma. ed. Madrid: Elsevier SA; 2005. p.

  6. Santos VP, Caffaro RA, Pozzan G, Saieg MA, Castelli V. Comparative histological study of artherosclerotic lesions and microvascular changes in amputed lower mibs of diabetic and non-diabetic patients. Arq Bras Endocrinol Metabol. 2008 ; 52 (7): 1115-23.

  7. Kramer Ck, Leitao CB, Pinto LC, Bolson P, Boza J, Silveiro SP, et al. Risk factors for micro and macrovascular disease in black and white patients with type 2 Diabetes mellitus. Rev Assoc Med Bras. 2009 ; 55 (3): 308-14.

  8. Figuerola D, Reynals E. Diabetes mellitus. In: Farreras Valentí P, Rozman C. Medicina Interna. 13ra. ed. Madrid: Mosbi; 1995. p. 1933-68.

  9. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin dependent diabetes mellitus. N Engl J Med. 1993 ; 329 (14): 977-86.

  10. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatments and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998 ; 352 (9131): 837-53.

  11. Villanueva V. Enfoque práctico de las complicaciones crónicas de la Diabetes Mellitus. Rev Pos Via Cát Med. 2003 ; 1 (130): 1-18.

  12. Mahía M, Pérez L. La diabetes mellitus y sus complicaciones vasculares: un problema social de salud. Rev Cubana Angiol y Cir Vasc. 2000 ; 1 (1): 68-73.

  13. Corrêa ML, Vieira SM. A predisposiçao genética para o desenvolvimento da microangiopatia no DM1. Arq Bras Endocrinol Metab. 2008 ; 52 (2): 375-86.

  14. Emanueli C, Salis MB, Pinna A, Stacca T, Milia A F , S p a n o A , e t a l . P r e v e n t i o n o f diabetes-induced microangiopathy by human tissue kallikrein gene transfer. Circulation. 2002 ; 106 (8): 993-9.

  15. Cardellá L, Hernández R. Estructura y función de las biomoléculas. Bioquímica Médica. La Habana: ECIMED; 1999. p. 105-12.

  16. Olmos P, Araya-Del-Pino A, González C, Laso P, Irribarra V, Rubio L. Fisiopatología de la retinopatía y nefropatía diabéticas. Rev méd Chile. 2009 ; 137 (10): 1375-84.

  17. Cardellá L, Hernández R. Digestión y absorción de los glúcidos. Bioquímica Médica. La Habana: ECIMED; 1999. p. 715.

  18. Das Evcimen ND, King GL. The role of protein kinase C activation and the vascular complications of diabetes. Pharmacol Res. 2007 ; 55 (6): 498-510.

  19. L a v r e n t y e v E N , M a l i k K U . H i g h glucose-induced Nox1-derived superoxides downregulate PKC-βII, which subsequently decreases ACE2 expression and ANG(1-7) formation in rat VSMCs. Am J Physiol Heart Circ Physiol. 2009 ; 296 (1): H106-18.

  20. Sutera SP, Chang K, Marvel J, Williamson JR. Concurrent increases in regional hematocrit and blood flow in diabetic rats: prevention by sorbinil. Am J Physiol Heart Circ Physiol. 1992 ; 263 (3 Pt 2): H945-50.

  21. González R, Buchaca E, Licea ME. Fisiopatología y progresión de las personas con prediabetes. Rev Cubana Endocrinol. 2011 ; 22 (1): 1-7.

  22. Cruz J, Licea ME. Glucosilación no enzimática y complicaciones crónicas de la diabetes mellitus. Rev Cubana Endocrinol. 2010 ; 21 (2): 223-55.

  23. Janghorbani M, Amini M. Patterns and predictors of long-term glycemic control in patients with type 2 diabetes. Endocrinol. 2012 ; 526824. doi: 10.5402/2012/526824:

  24. Jakus V, Rietbrock N. Advanced glycation end-products and the progress of diabetic vascular complications. Physiol Res. 2004 ; 53 (2): 131-42.

  25. Guo X, Wang L, Chen B, Li Q, Wang J, Zhao M, et al. ERM protein moesin is phosphorylated by advanced glycation end products and modulates endothelial permeability. Am J Physiol Heart Circ Physiol. 2009 ; 297 (1): H238-46.

  26. Bagi Z, Toth E, Koller A, Kaley G. Microvascular dysfunction after transient high glucose is caused by superoxide-dependent reduction in the bioavailability of NO and BH(4). Am J Physiol Heart Circ Physiol. 2004 ; 287 (2): H626-33.

  27. Bishara NB, Ding H. Glucose enhances expression of TRPC1 and calcium entry in endothelial cells. Am J Physiol Heart Circ Physiol. 2010 ; 298 (1): H171-8.

  28. Abi-Chahin TC, Hausen Mde A, Mansano CM, Halfoun VL. Microvascular reactivity in type 1 diabetics. Arq Bras Endocrinol Metabol. 2009 ; 53 (6): 741-6.

  29. Houben AJ, Schaper NC, Haan CH, Huvers FC, Slaaf DW, Leeuw PW, et al. Local 24-h h y p e r g l y c e m i a d o e s n o t a f f e c t endothelium-dependent or -independent vasoreactivity in humans. Am J Physiol. 1996 ; 270 (6 Pt 2): H2014-20.

  30. Padilla DJ, McDonough P, Behnke BJ, Kano Y, Hageman KS, Musch TI, et al. Effects of Type II diabetes on capillary hemodynamics in skeletal muscle. J Physiol Heart Circ Physiol. 2006 ; 291 (5): H2439-44.

  31. Álvarez N. Retinopatía Diabética. Bol Esc Med. 2006 ; 31 (2): 1-90.

  32. Lee IG, Chae SL, Kim JC. Involvement of circulating endothelial progenitor cells and vasculogenic factors in the pathogenesis of diabetic retinopathy. Eye. 2006 ; 20 (5): 546-52.

  33. Fadini GP, Mancuso P, Bertolini F, de Kreutzenberg S, Avogaro A. Amelioration of Glucose Control Mobilizes Circulating Pericyte Progenitor Cells in Type 2 Diabetic Patients with Microangiopathy. Exp Diab Res. 2012 ; 12 (1): 1-8.

  34. Macía Heras M, Macía Jerez M, Coronel F. Nefropatía diabética: fisiopatología y curso clínico. Nefrología. 2001 ; 21 (3): 1-10.




2020     |     www.medigraphic.com

Mi perfil

C?MO CITAR (Vancouver)

Finlay. 2013;3