Glycosylation end products in serum homocysteine levels and vascular endothelial dysfunction and the relationship between.docVIP

 PAGE \* MERGEFORMAT 9 Glycosylation end products in serum homocysteine levels and vascular endothelial dysfunction and the relationship between Study: Hu Kai, Zhang Kang Xuejun Sun Zilin [Abstract] Objective To investigate the chronic complications of type 2 diabetes and patients with advanced glycation end products (AGEs and homocysteine (HCY levels in endothelial dysfunction. METHODS flow injection analysis of serum AGEs levels high performance liquid chromatography with electrochemical detection of serum HCY levels. nitrate reductase method and radioimmunoassay of serum nitric oxide were detected (NO and endothelin (ET levels. Results were serum HCY, AGES, ET were significantly higher in the control group (P lt;0.01 or P lt;0.05. Serum NO levels were significantly lower than the control group (P lt;0.01 or P lt;0.05. diabetic vascular disease HCY, ET levels were significantly higher than microvascular disease group (P lt;0.01 or P lt;0.05. diabetes and complications in patients with HCY and serum AGEs were positively correlated with ET (r values were 0.267, P lt;0.01 and 0.153, P lt;0.05, but no correlation with NO (r values were 0.021 and 0.036, both Pgt; 0.05. Conclusions AGES high Hcy and diabetes and its complications are important risk factors for vascular disease and both may have synergistic effects. Hcy may be related to diabetic vascular disease associated with a greater degree. Hcy and AGEs may be the main reason for the increase in the level of ET. [Keywords:] diabetes, type 2, advanced glycation end products, homocysteine, nitric oxide, endothelin Recent studies show that the (1,2) glycation end products (AGEs) in receptor-dependent and non-receptor-mediated type of form that barriers lead to endothelial cell function and accelerate the process of atherosclerosis. The same type of cysteine acid (Hcy) by oxidative stress, stimulation of vascular smooth muscle cell proliferation, and many other mechanisms cause endothelial cell dysfunc