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Chinese Journal of Natural Medicines (English Ed.) ; (6): 844-855, 2016.
Article Dans Anglais | WPRIM | ID: wpr-812568

Résumé

The aim of this study was to investigate the effects of high-advanced glycation end products (AGEs) diet on diabetic vascular complications. The Streptozocin (STZ)-induced diabetic mice were fed with high-AGEs diet. Diabetic characteristics, indicators of renal and cardiovascular functions, and pathohistology of pancreas, heart and renal were evaluated. AGEs/RAGE/ROS pathway parameters were determined. During the experiments, the diabetic mice exhibited typical characteristics including weight loss, polydipsia, polyphagia, polyuria, high-blood glucose, and low-serum insulin levels. However, high-AGEs diet effectively aggravated these diabetic characteristics. It also increased the 24-h urine protein levels, serum levels of urea nitrogen, creatinine, c-reactive protein (CRP), low density lipoprotein (LDL), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in the diabetic mice. High-AGEs diet deteriorated the histology of pancreas, heart, and kidneys, and caused structural alterations of endothelial cells, mesangial cells and podocytes in renal cortex. Eventually, high-AGEs diet contributed to the high-AGE levels in serum and kidneys, high-levels of reactive oxygen species (ROS) and low-levels of superoxide dismutase (SOD) in serum, heart, and kidneys. It also upregulated RAGE mRNA and protein expression in heart and kidneys. Our results showed that high-AGEs diet deteriorated vascular complications in the diabetic mice. The activation of AGEs/RAGE/ROS pathway may be involved in the pathogenesis of vascular complications in diabetes.


Sujets)
Animaux , Humains , Mâle , Souris , Diabète expérimental , Métabolisme , Angiopathies diabétiques , Génétique , Métabolisme , Régime alimentaire , Produits terminaux de glycation avancée , Métabolisme , Interleukine-6 , Métabolisme , Rein , Métabolisme , Souris de lignée C57BL , Stress oxydatif , Pancréas , Métabolisme , Espèces réactives de l'oxygène , Métabolisme , Récepteur spécifique des produits finaux de glycosylation avancée , Génétique , Métabolisme , Superoxide dismutase , Métabolisme , Facteur de nécrose tumorale alpha , Métabolisme
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