SUPPRESSION OF ADVANCED GLYCATION AND LIPOXIDATION END PRODUCTS BY AN ANGIOTENSIN II TYPE-1 RECEPTOR BLOCKER IN ESSENTIAL HYPERTENSION WITH TYPE-2 DIABETES MELLITUS

2004 ◽  
Vol 22 (Suppl. 1) ◽  
pp. S185
Author(s):  
Y Ono ◽  
K Mizuno ◽  
M Takahashi ◽  
Y Miura
2018 ◽  
Vol 20 (4) ◽  
pp. 535-540 ◽  
Author(s):  
Mohammed Alrabiah ◽  
Khulud Abdulrahman Al-Aali ◽  
Zeyad H. Al-Sowygh ◽  
Abdulelah M. Binmahfooz ◽  
Sameer A Mokeem ◽  
...  

2019 ◽  
Vol 16 (5) ◽  
pp. 458-465 ◽  
Author(s):  
Eugenia Gkaliagkousi ◽  
Barbara Nikolaidou ◽  
Eleni Gavriilaki ◽  
Antonios Lazaridis ◽  
Efthalia Yiannaki ◽  
...  

Aim: To investigate the thrombotic microenvironment in early stages of type 2 diabetes mellitus measuring platelet-derived, endothelial-derived and erythrocyte-derived microvesicles. Methods: We recruited 50 newly diagnosed type 2 diabetes mellitus patients who did not receive glucose-lowering treatment except for metformin and 25 matched non-type 2 diabetes mellitus volunteers. Microvesicles were measured with flow cytometry, glycated haemoglobin with high-performance liquid chromatography and advanced glycation end products with enzyme-linked immunosorbent assay. Results: Type 2 diabetes mellitus patients showed significantly higher levels of platelet-derived microvesicles [195/μL (115–409) vs 110/μL (73–150), p = 0.001] and erythrocyte-derived microvesicles [26/μL (9–100) vs 9/μL (4–25), p = 0.007] compared to non-type 2 diabetes mellitus individuals. Platelet-derived microvesicles were positively associated with fasting blood glucose ( p = 0.026) and glycated haemoglobin ( p = 0.002). Erythrocyte-derived microvesicles were also positively associated with fasting blood glucose ( p = 0.018) but not with glycated haemoglobin ( p = 0.193). No significant association was observed between platelet-derived microvesicles ( p = 0.126) or erythrocyte-derived microvesicles ( p = 0.857) and advanced glycation end products. Erythrocyte-derived microvesicles predicted the presence of type 2 diabetes mellitus, independently of platelet-derived microvesicles. Conclusion: In newly diagnosed type 2 diabetes mellitus, ongoing atherothrombosis is evident during the early stages as evidenced by increased microvesicles levels. Furthermore, the association with glycemic profile suggests that microvesicles represent not only a novel mechanism by which hyperglycemia amplifies thrombotic tendency in type 2 diabetes mellitus but also early markers of thrombosis highlighting the need for earlier management of hyperglycemia.


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