Advanced Glycation End Products, Measured as Skin Autofluorescence, During Normal Pregnancy and Pregnancy Complicated by Diabetes Mellitus

2012 ◽  
Vol 14 (12) ◽  
pp. 1134-1139 ◽  
Author(s):  
Wendela L. de Ranitz-Greven ◽  
Lotte Kaasenbrood ◽  
Wendy K. Poucki ◽  
Jeanette Hamerling ◽  
Dieuwke C. Bos ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Advanced Glycation End Products ◽  
Normal Pregnancy ◽  
Skin Autofluorescence ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Role of Advanced Glycation End Products in Assessment of Diabetes Mellitus as a Risk Factor for Retinal Vein Occlusion

2021 ◽  
Vol 11 (17) ◽  
pp. 7934
Author(s):  
Karolina Kaźmierczak ◽  
Paweł Żuchowski ◽  
Katarzyna Łapińska-Duczmal ◽  
Katarzyna Zabel ◽  
Zofia Sikorska ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Retinal Vein Occlusion ◽  
Advanced Glycation End Products ◽  
Systemic Hypertension ◽  
Control Group ◽  
Skin Autofluorescence ◽  
Advanced Glycation ◽  
Vein Occlusion ◽  
Glycation End Products ◽  
End Products

Aim: In this study, we aimed to assess the correlation between diabetes mellitus (DM) and the retinal vein occlusion (RVO) based on skin autofluorescence (SAF) measurement, which reflects the accumulation of advanced glycation end products (AGE) in patients who have undergone an episode of central retinal vein occlusion (CRVO) or branch retinal vein occlusion (BRVO). Material and methods: In total, 23 patients (16 males, 7 females) with RVO were included in this study. Among these 23 participants, 12 (52%) had been diagnosed with CRVO and 11 (48%) with BRVO. The control group consisted of 14 healthy volunteers (11 females, 3 males). To calculate the risk of cardiovascular diseases (CVD) and DM, we conducted SAF examinations. We compared the SAF levels in three groups of patients: (1) with CRVO, (2) with BRVO, and (3) the control group. Basic demographic and clinical information and detailed history of the concurrent diagnoses of systemic diseases, such as systemic hypertension (HTN), DM, hyperlipidemia (HL), and heart diseases, were obtained. Results: In total, 10 (43.5%) patients were diagnosed with DM, 6 (55%) in the BRVO group and 4 (33%) in the CRVO group. The mean SAF value was significantly higher in the BRVO group than in the control group (2.64 a.u. and 2.35 a.u., respectively) (p = 0.023). More patients with risk of DM were identified in the CRVO group than in the BRVO group (p = 0.024). Conclusions: The advanced glycation end products (AGE) in the skin autofluorescence (SAF) is a viable method of evaluating the risk of DM in patients with RVO. We confirmed a correlation between RVO and DM, which was significantly pronounced in the CRVO form, although further carefully devised studies on the relationship between RVO and DM with a larger number of responders should be conducted in the future.

scholarly journals Advanced glycation end products induce a prothrombotic phenotype in mice via interaction with platelet CD36

Blood ◽  
2012 ◽  
Vol 119 (25) ◽  
pp. 6136-6144 ◽  
Author(s):  
Weifei Zhu ◽  
Wei Li ◽  
Roy L. Silverstein
Keyword(s):  
Diabetes Mellitus ◽  
Mouse Models ◽  
Advanced Glycation End Products ◽  
Vascular Complications ◽  
Dependent Manner ◽  
Advanced Glycation ◽  
Drug Induced ◽  
Glycation End Products ◽  
End Products

Abstract Diabetes mellitus has been associated with platelet hyperreactivity, which plays a central role in the hyperglycemia-related prothrombotic phenotype. The mechanisms responsible for this phenomenon are not established. In the present study, we investigated the role of CD36, a class-B scavenger receptor, in this process. Using both in vitro and in vivo mouse models, we demonstrated direct and specific interactions of platelet CD36 with advanced glycation end products (AGEs) generated under hyperglycemic conditions. AGEs bound to platelet CD36 in a specific and dose-dependent manner, and binding was inhibited by the high-affinity CD36 ligand NO2LDL. Cd36-null platelets did not bind AGE. Using diet- and drug-induced mouse models of diabetes, we have shown that cd36-null mice had a delayed time to the formation of occlusive thrombi compared with wild-type (WT) in a FeCl3-induced carotid artery injury model. Cd36-null mice had a similar level of hyperglycemia and a similar level of plasma AGEs compared with WT mice under this condition, but WT mice had more AGEs incorporated into thrombi. Mechanistic studies revealed that CD36-dependent JNK2 activation is involved in this prothrombotic pathway. Therefore, the results of the present study couple vascular complications in diabetes mellitus with AGE-CD36–mediated platelet signaling and hyperreactivity.

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