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Alexis Guerin-Dubourg [1; 2] and Maxime Cournot [1; 2; 3] and Cynthia Planesse [1] and Xavier Debussche [3] and Olivier Meilhac [1; 3] and Philippe Rondeau [1] and Emmanuel Bourdon [1]

Academic Editor: Kamel Mohammedi

1, Université de La Réunion, INSERM, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Saint-Denis de La Réunion, France, inserm.fr

2, Centre Hospitalier Gabriel Martin, Saint-Paul, France

3, Centre Hospitalier Universitaire de La Réunion, Saint Denis, France, chu-reunion.fr

Received May 22, 2017; Revised Aug 11, 2017; Accepted Sep 10, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Type 2 diabetes mellitus (T2DM) is a metabolic disease which has reached pandemic proportions and is considered as one of the world’s most important causes of healthcare expenditure, disability, and mortality. Enhanced morbidity in diabetes is mainly associated with micro- and macrovascular complications [1]. Indeed, T2DM could double the risk of developing cardiovascular diseases (CVD) including stroke and myocardial infarction, which represent the leading cause of mortality in western and developing countries [2]. In Réunion Island, a French overseas territory, diabetes prevalence is particularly high (>20% of adult people) and is associated with a higher vascular disease-related mortality (×2) when compared to mainland France [3].

Glycation is clearly identified as a deleterious phenomenon in diabetic complications and the association with oxidative stress seems to be deleterious too [4, 5]. One of the underlying features of hyperglycaemia is the excessive nonenzymatic glycation of the two main circulating proteins: haemoglobin and albumin. This chemical process consists in a complex cascade of reactions between glucose or derivatives with proteins, yielding a heterogeneous class of compounds termed advanced glycation end-products (AGE) [6]. Glycation process, in conjunction with oxidative stress named “glycoxidation” can cause structural and functional impairments of plasma proteins in particular albumin [7–9] and was involved in pathophysiological mechanism of vascular diseases in T2DM [10, 11]. Many clinical studies have suggested glycated albumin (GA) and ischemia-modified albumin (IMA) as additional and/or alternative plasma biomarkers of poor glycemic control, redox state, and glycation levels in diabetic subjects [12–14]. Similarly, the redox state of plasma thiols could also be used as a...
   
 
     
 
 
   
   
     
         
       
         
     
         
   
         
 
         
   
 
       
 
     
         
       
         
     
         
   
         
 
         
 

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