Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2013, Article ID 690650, 9 pages
http://dx.doi.org/10.1155/2013/690650
Research Article

Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions

1Laboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, Portugal
2Center of Ophthalmology, IBILI, Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, Portugal

Received 14 January 2013; Revised 26 February 2013; Accepted 1 March 2013

Academic Editor: Adelino Leite Moreira

Copyright © 2013 Tiago Rodrigues et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. P. Matafome, D. Santos-Silva, J. Crisóstomo et al., “Methylglyoxal causes structural and functional alterations in adipose tissue independently of obesity,” Archives of Physiology and Biochemistry, vol. 118, pp. 58–68, 2012. View at Google Scholar
  2. A. Goldin, J. A. Beckman, A. M. Schmidt, and M. A. Creager, “Advanced glycation end products: sparking the development of diabetic vascular injury,” Circulation, vol. 114, no. 6, pp. 597–605, 2006. View at Publisher · View at Google Scholar · View at Scopus
  3. A. Negre-Salvayre, R. Salvayre, N. Augé, R. Pamplona, and M. Portero-Otín, “Hyperglycemia and glycation in diabetic complications,” Antioxidants and Redox Signaling, vol. 11, no. 12, pp. 3071–3109, 2009. View at Publisher · View at Google Scholar · View at Scopus
  4. G. H. Goossens, “The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance,” Physiology and Behavior, vol. 94, no. 2, pp. 206–218, 2008. View at Publisher · View at Google Scholar · View at Scopus
  5. J. Kim, O. S. Kim, C.-S. Kim, E. Sohn, K. Jo, and J. S. Kim, “Accumulation of argpyrimidine, a methylglyoxal-derived advanced glycation end product, increases apoptosis of lens epithelial cells both in vitro and in vivo,” Experimental & Molecular Medicine, vol. 44, pp. 167–175, 2012. View at Google Scholar
  6. A. K. Berner, O. Brouwers, R. Pringle et al., “Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology,” Diabetologia, vol. 55, pp. 845–854, 2012. View at Google Scholar
  7. C. Sena, P. Matafome, J. Crisَstomo et al., “Methylglyoxal promotes oxidative stress and endothelial dysfunction,” Pharmacological Research, vol. 65, pp. 497–506, 2012. View at Google Scholar
  8. A. V. Cantero, M. Portero-Otín, V. Ayala et al., “Methylglyoxal induces advanced glycation end product (AGEs) formation and dysfunction of PDGF receptor-β: implications for diabetic atherosclerosis,” FASEB Journal, vol. 21, no. 12, pp. 3096–3106, 2007. View at Publisher · View at Google Scholar · View at Scopus
  9. P. A. Voziyan and B. G. Hudson, “Pyridoxamine as a multifunctional pharmaceutical: targeting pathogenic glycation and oxidative damage,” Cellular and Molecular Life Sciences, vol. 62, no. 15, pp. 1671–1681, 2005. View at Publisher · View at Google Scholar · View at Scopus
  10. V. K. Pedchenko, S. V. Chetyrkin, P. Chuang et al., “Mechanism of perturbation of integrin-mediated cell-matrix interactions by reactive carbonyl compounds and its implication for pathogenesis of diabetic nephropathy,” Diabetes, vol. 54, no. 10, pp. 2952–2960, 2005. View at Publisher · View at Google Scholar · View at Scopus
  11. T. O. Metz, N. L. Alderson, S. R. Thorpe, and J. W. Baynes, “Pyridoxamine, an inhibitor of advanced glycation and lipoxidation reactions: a novel therapy for treatment of diabetic complications,” Archives of Biochemistry and Biophysics, vol. 419, no. 1, pp. 41–49, 2003. View at Publisher · View at Google Scholar · View at Scopus
  12. F. Depeint, W. R. Bruce, N. Shangari, R. Mehta, and P. J. O'Brien, “Mitochondrial function and toxicity: role of B vitamins on the one-carbon transfer pathways,” Chemico-Biological Interactions, vol. 163, no. 1-2, pp. 113–132, 2006. View at Publisher · View at Google Scholar · View at Scopus
  13. E. A. Muellenbach, C. J. Diehl, M. K. Teachey et al., “Interactions of the advanced glycation end product inhibitor pyridoxamine and the antioxidant α-lipoic acid on insulin resistance in the obese Zucker rat,” Metabolism, vol. 57, no. 10, pp. 1465–1472, 2008. View at Publisher · View at Google Scholar · View at Scopus
  14. F. Zheng, Y. J. Zeng, A. R. Plati et al., “Combined AGE inhibition and ACEi decreases the progression of established diabetic nephropathy in B6 db/db mice,” Kidney International, vol. 70, no. 3, pp. 507–514, 2006. View at Publisher · View at Google Scholar · View at Scopus
  15. E. M. Muellenbach, C. J. Diehl, M. K. Teachey et al., “Metabolic interactions of AGE inhibitor pyridoxamine and antioxidant α-lipoic acid following 22weeks of treatment in obese Zucker rats,” Life Sciences, vol. 84, no. 15-16, pp. 563–568, 2009. View at Publisher · View at Google Scholar · View at Scopus
  16. X. Wang, K. Desai, T. Chang, and L. Wu, “Vascular methylglyoxal metabolism and the development of hypertension,” Journal of Hypertension, vol. 23, no. 8, pp. 1565–1573, 2005. View at Google Scholar · View at Scopus
  17. J. Berlanga, D. Cibrian, I. Guillén et al., “Methylglyoxal administration induces diabetes-like microvascular changes and perturbs the healing process of cutaneous wounds,” Clinical Science, vol. 109, no. 1, pp. 83–95, 2005. View at Publisher · View at Google Scholar · View at Scopus
  18. J. M. Onorato, A. J. Jenkins, S. R. Thorpe, and J. W. Baynes, “Pyridoxamine, an inhibitor of advanced glycation reactions, inhibits advanced lipoxidation reactions: mechanism of action of pyridoxamine,” Journal of Biological Chemistry, vol. 275, no. 28, pp. 21177–21184, 2000. View at Publisher · View at Google Scholar · View at Scopus
  19. R. G. Khalifah, Y. Chen, and J. J. Wassenberg, “Post-Amadori AGE inhibition as a therapeutic target for diabetic complications: a rational approach to second-generation Amadorin design,” Annals of the New York Academy of Sciences, vol. 1043, pp. 793–806, 2005. View at Publisher · View at Google Scholar · View at Scopus
  20. A. Yuen, C. Laschinger, I. Talior et al., “Methylglyoxal-modified collagen promotes myofibroblast differentiation,” Matrix Biology, vol. 29, no. 6, pp. 537–548, 2010. View at Publisher · View at Google Scholar · View at Scopus
  21. C. F. Bento, R. Fernandes, P. Matafome, C. Sena, R. Seia, and P. Pereira, “Methylglyoxal-induced imbalance in the ratio of vascular endothelial growth factor to angiopoietin 2 secreted by retinal pigment epithelial cells leads to endothelial dysfunction,” Experimental Physiology, vol. 95, no. 9, pp. 955–970, 2010. View at Publisher · View at Google Scholar · View at Scopus
  22. W. H. Chan, H. J. Wu, and N. H. Shiao, “Apoptotic signaling in methylglyoxal-treated human osteoblasts involves oxidative stress, c-Jun N-terminal kinase, caspase-3, and p21-activated kinase 2,” Journal of Cellular Biochemistry, vol. 100, no. 4, pp. 1056–1069, 2007. View at Publisher · View at Google Scholar · View at Scopus
  23. J. Kim, N. H. Kim, E. Sohn, C. S. Kim, and J. S. Kim, “Methylglyoxal induces cellular damage by increasing argpyrimidine accumulation and oxidative DNA damage in human lens epithelial cells,” Biochemical and Biophysical Research Communications, vol. 391, no. 1, pp. 346–351, 2010. View at Publisher · View at Google Scholar · View at Scopus