scholarly journals Concentration of Endogenous Secretory Receptor for Advanced Glycation End Products and Matrix Gla Protein in Controlled and Uncontrolled Type 2 Diabetes Mellitus Patients

2013 ◽  
Vol 5 (1) ◽  
pp. 31
Author(s):  
Dwi Yuniati Daulay ◽  
Suryani As'ad ◽  
Ali Aspar Mappahya ◽  
Andi Wijaya

BACKGROUND: Advanced glycation end products (AGE) and their receptor (RAGE) system play an important role in the development of diabetic vascular complications. Recently, an endogenous secretory RAGE (esRAGE) has been identified as a novel splice variant, which lacks the transmembrane domain and is secreted in human sera. Interestingly, it was reported that esRAGE binds AGE ligands and neutralizes AGE actions. Many studies have reported that diabetes mellitus correlates with vascular calcification event and increases progressively in uncontrolled diabetes. Matrix Gla Protein (MGP) is known to act as an inhibitor in vascular calcification. The aim of this study was to observe progress of vascular calcification in uncontrolled diabetes patient by biochemical markers MGP as inhibitor in vascular calcification, via mechanism of AGEs.METHODS: This study was an observational study with cross sectional design on adult type 2 diabetic male patients who were defined by the 2011 Indonesian diabetes mellitus consensus criteria.RESULTS: The results of this study showed that there was a positive significant correlation between esRAGE and HbA1C (r=0.651, p=0.009), and negative correlation between MGP and HbA1C (r=-0.465, p=0.081) in controlled diabetes group. In uncontrolled diabetes group there was a positive significant correlation between MGP and HbA1C (r=0.350, p=0.023), despite the fact esRAGE showed no significant correlation with HbA1C. There was no significant difference in level of esRAGE and MGP in controlled and uncontrolled diabetes group, but MGP showed lower level in uncontrolled diabetes group, contrary to esRAGE that had higher concentration.CONCLUSION: In diabetes condition, complications of vascular calcification are caused by the mechanism of increased AGE formation represented by esRAGE. In diabetes control it is very important to keep the blood vessels from complications caused by vascular calcification.KEYWORDS: type 2 diabetes mellitus, vascular calcification, esRAGE, MGP, HbA1C

2010 ◽  
Vol 2 (2) ◽  
pp. 40
Author(s):  
Dwi Yuniati Daulay ◽  
Marsetio Donosepoetro ◽  
Sutomo Kasiman

BACKGROUND: Many studies have reported that diabetes mellitus correlates with vascular calcification event that increases progressively in uncontrolled diabetes. Osteoprotegerin (OPG) is known to act as a promoter in vascular calcification, contrary to Matrix Gla Protein (MGP), which is an inhibitor in vascular calcification. The aim of this study was to observe the progress of vascular calcification in uncontrolled diabetes patients by assessing biochemical markers OPG as promoter and MGP as inhibitor in vascular calcification.METHODS: This was an observational study with cross sectional design on adult male patients with type 2 diabetes mellitus, defined by DM Consensus Criteria Indonesia, 2006.RESULTS: The results of this study showed that there was a positive significant correlation between OPG and HbA1c (r=0.261, p=0.030), in contrast with MGP that showed no significant correlation with HbA1c. OPG also correlated significantly with Fasting Plasma Glucose (r=0.261, p=0.014). In uncontrolled diabetes group there was positive significant correlation between OPG and HbA1c (r=0.397, p=0.014). There was no significant difference found in the levels of OPG in controlled and uncontrolled diabetes groups (p=0.567), but OPG/MGP index showed higher difference (p=0.259). The OPG/MGP index also had positive significant correlation with HbA1c (r=0.285, p=0.018) and Fasting Plasma Glucose (r=0.313, p=0.009).CONCLUSIONS: This study suggested progress to vascular calcification in uncontrolled type 2 diabetes mellitus. The use of vascular calcification biomarkers are recommended to predict/detect vascular calcification event in type 2 diabetes mellitus patients.KEYWORDS: type 2 diabetes mellitus, vascular calcification, OPG, MGP, HbA1c


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.


Author(s):  
Debie Anggraini ◽  
Rismawati Yaswir ◽  
Lillah Lillah ◽  
Husni Husni

Nefropati diabetik merupakan komplikasi mikrovaskular di pasien Diabetes Melitus (DM) yang menyebabkan End Stage RenalDisease (ESRD). Proses glikasi non-enzimatik asam amino bebas di hiperglikemia kronis menghasilkan advanced glycation end-products(AGEs). Advanced glycation end-products dimetabolisme di ginjal sehingga terjadi penumpukan yang memicu kerusakan glomerulusginjal. Advanced glycation end-products terbukti berperan dalam perjalanan penyakit nefropati diabetik. Pemeriksaan mikroalbuminuriadengan rasio air kemih albumin kreatinin merupakan pemeriksaan yang disarankan untuk mendeteksi nefropati lebih awal. Tujuanpenelitian ini untuk mengetahui kenasaban kadar AGEs dengan rasio air kemih albumin kreatinin di pasien DM tipe 2. Penelitian inimenggunakan metode analitik dengan desain potong lintang di 30 orang pasien DM tipe 2 yang memenuhi patokan kesertaan dannonkesertaan serta melakukan pemeriksaan darah di Instalasi Laboratorium Sentral RSUP Dr. M. Djamil Padang masa waktu Mei2015-Maret 2016. Pemeriksaan kadar AGEs dilakukan dengan metode sandwich ELISA. Pemeriksaan mikroalbumin air kemih dilakukandengan metode imunoturbidimetri. Data dianalisis dengan uji kenasaban Spearman, bermakna jika p<0,05. Rerata kadar AGEs di DMtipe 2 adalah 1052,18±750,25 ng/L. Rerata nilai rasio air kemih albumin kreatinin di pasien DM tipe 2 adalah 23,77±16,58 mg/g.Uji kenasaban Spearman menunjukkan kenasaban sangat kuat antara kadar AGEs dan rasio air kemih albumin kreatinin dengannilai r=0,85 dan nilai p<0,05. Terdapat kenasaban sangat kuat antara kadar AGEs dengan rasio air kemih albumin kreatinin di DMtipe 2.


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