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LV Xing, LV Gao-Hong, DAI Guo-Ying, SUN Hong-Mei, XU Hui-Qin. Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway[J]. 中国天然药物, 2016, 14(11): 844-855.
引用本文: LV Xing, LV Gao-Hong, DAI Guo-Ying, SUN Hong-Mei, XU Hui-Qin. Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway[J]. 中国天然药物, 2016, 14(11): 844-855.
LV Xing, LV Gao-Hong, DAI Guo-Ying, SUN Hong-Mei, XU Hui-Qin. Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway[J]. Chinese Journal of Natural Medicines, 2016, 14(11): 844-855.
Citation: LV Xing, LV Gao-Hong, DAI Guo-Ying, SUN Hong-Mei, XU Hui-Qin. Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway[J]. Chinese Journal of Natural Medicines, 2016, 14(11): 844-855.

Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway

Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway

  • 摘要: 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- (TNF-), 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.

     

    Abstract: 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- (TNF-), 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.

     

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