Aspectos moleculares del daño tisular inducido por la hiperglucemia crónica

Margarita Díaz-Flores, Luis Arturo Baiza-Gutman, Miguel Angel Ibáñez-Hernández, Dalila Pascoe-Lira, Alberto M. Guzmán-Greenfel, Jesús Kumate-Rodríguez

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20 Citas (Scopus)

Resumen

The knowledge of the molecular basis of diabetes mellitus physiopathology will allow improvements in treatment or prevention of the disease. Diabetes mellitus is a complex disease in which hyperglycemia leads to complications in several organs. In this condition, there is increase in reactive oxygen species (ROS) as a result of glucose autooxidation; its metabolism produces accumulation of metabolites such as fructose, sorbitol, and triose phosphate. The latter generates α oxoaldehydes with high capacity to produce protein glycation and oxidative stress. Moreover, there is an increase in synthesis of diacylglycerol from triose phosphate, which activates protein kinase C. On the other hand, alteration of normal ratio between reduced and oxidized niacinamide nucleotides leads to low efficiency of antioxidative systems. Finally, this metabolic dysregulation causes alteredsignal transduction, abnormal gene expression, and tissue damage, resulting in development of diabetic complications.

Título traducido de la contribuciónMolecular aspects of chronic hyperglycemia-induced tissue damage
Idioma originalEspañol
Páginas (desde-hasta)437-447
Número de páginas11
PublicaciónGaceta Medica de Mexico
Volumen140
N.º4
EstadoPublicada - jul. 2004

Palabras clave

  • AGES
  • Chronic complications
  • Diabetes mellitus
  • Diacylglycerol
  • Hexosamines
  • Oxidative stress
  • Protein kinase C
  • Sorbitol

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