ROLE OF GLYCATION END-PRODUCTS BLOCKERS IN THE DEVELOPMENT OF NEUROLOGIC COMPLICATIONS OF DIABETES MELLITUS


Cite item

Full Text

Abstract

The article considers the pathogenesis of neurological complications of diabetes mellitus in terms of the damaging effect of hyperglycemia and activation of pathological ways of glucose utilization. One of the most important mechanisms of tissue damage by glucose is the formation of advanced glycation end-products (AGEP) and their predecessors. B vitamins, including fat-soluble thiamine analogue benfotiamine, play an important role in the treatment of diabetic neuropathy. It was shown that benfotiamine is a neurotropic substance with the ability to block excessive formation of the AGEP. Benfotiamine with pyridoxine are components of drug Milgamma compositum. Clinical evidences for the therapeutic effect of benfotiamine in the treatment of diabetic neuropathy are presented.

References

  1. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 2001;414:813-20.
  2. Brownlee M. The pathobiology of diabetic complications. A unifying mechanism. Diabetes 2005;54:1615-25.
  3. Berrone E, Beltramo E, Solimine C, et al. Regulation of intracellular glucose and polyol pathway by thiamine and benfothiamine in vascular cells cultured in high glucose. J Biol Chem 2006;281(14):9307-13.
  4. Beltramo E, Berrone E, Tarallo S, et al. Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications. Acta Diabetol 2008;45:131-41.
  5. Chalk C, Benstead TJ, Moore F. Aldose reductase inhibitors for the treatment of diabetic polyneuropathy. Cochrane Database Syst Rev 2007;4:CD004572.
  6. Du X, Edelstein D, Rossetti L, et al. Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing SP1 glycosylation. Proc Nat Acad Sci USA 2000;97:12222-26.
  7. Du X, Matsumura T, Edelstein D, et al. Inhibition of GADPH activity by poly-(ADP ribose)-polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest 2003;112:1049-57.
  8. Mauro GL, Martorana U, Cataldo L, et al. Vitamin B12 in low back pain: a randomised, double-blind, placebo-controlled study. Eur Rev Med Pharmacol Sci 2000;4:53-8.
  9. Mooney S. Leuendorf JE. Hendrickson C, Hellmann H. Vitamin B6 a long known compound of surprising complexity. Molecules 2009:14(1):329-51.
  10. MacKenzie KE, Wiltshire EJ, Gent R, et al. Folate and vitamin B6 rapidly normalize endothelial dysfunction in children with type 1 diabetes mellitus. Pediatrics 2006;118:242-53.
  11. Rabbani N, Alam SS, Riaz S, et al. High-dose thiamine therapy for pathients with type 2 diabetes and microalbuminuria: a pilot randomized, double-blind placebo-controlled pilot study. Diabetologia 2009;52(2):208-12.
  12. Russell JW, Fehtman EI. Impaired glucose tolerance - does it cause neuropathy? Muscle Nerve 2001;24(9):1109-10.
  13. Solomon LR. Disorders of cobalamin (vitamin B12) metabolism: emerging concepts in pathophisiology, diagnosis and treatment. Blood Rev 2007;21(3):113-30.
  14. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: Benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997;52:319-20.
  15. Nishikawa T, Edelstein D, Du X, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycemic damage. Nature 2000;404:787-90.
  16. Thornalley PJ. Glyoxalase I. Structure, function, and a critical role in the enzymatic defence against glycation. Biochem Soc Trans 2003;31:1343-48.
  17. Haupt E, Ledermann H, Kopcke W. Benfotiamine in the treatment of diabetic polyneuropathy-a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther 2005;43(2):71-77.
  18. Yang X, Ongusaha PP, Miles PD, et al. Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance. Nature 2008;451:964-69.
  19. Ihnat MA, Thorpe JE, Ceriello A. The "metabolic memory", the new challenge of diabetes. Diabet Med 2007;24:582-86.
  20. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med 2003;9:294-99.
  21. Du X, Edelstein D, Brownlee M. Oral benfotiamine plus α-lipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetologia 2008;51:1930-32.
  22. Jain SK, Lim G. Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na+/K+)-ATPase activity reduction in high glucose-treated human erythrocytes. Free Radic Biol Med 2001;30(3):232-37.
  23. Kelso BG, Brower JB, Targovnik JH, et al. Pyridoxine restores endothelial cell function in high glucose. Metab Syndr Relat Disord 2011;9(1):63-8.
  24. Winkler G, Pal B, Nagybeganyi E, et al. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Аneimittelforschung 1999;49(3):220-24.
  25. Маркина О.А. Значение лекарственной формы и пути введения витаминов группы В для обеспечения эффективного лечения диабетической полинейропатии // Клиническая фармакология и терапия 2003. № 2. C. 6-9.

Supplementary files

Supplementary Files
Action
1. JATS XML

Copyright (c) 2011 Bionika Media

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies