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      Endocan and a novel score for dyslipidemia, oxidative stress and inflammation (DOI score) are independently correlated with glycated hemoglobin (HbA 1c) in patients with prediabetes and type 2 diabetes

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          Abstract

          Introduction

          We aimed to examine serum endocan level and the summary involvement of dyslipidemia, oxidative stress (OS) and inflammation by calculation of its comprehensive score (i.e. Dyslipidemia-Oxy-Inflammation (DOI) score) in relation to glucoregulation in subjects with prediabetes and overt type 2 diabetes (T2D).

          Material and methods

          A total of 59 patients with prediabetes and 102 patients with T2D were compared with 117 diabetes-free controls. Glycated hemoglobin (HbA 1c), inflammation, OS and lipid parameters were measured. Associations of clinical data with HbA 1c level were tested with univariate and multivariate logistic ordinal regression analysis. HbA 1c as a dependent variable is given at the ordinal level (i.e. < 5.7%; 5.7–6.4%, > 6.4%, respectively).

          Results

          Endocan was significantly higher in the T2D group than in the controls. As endocan concentration rose by 1 unit, the probability for higher HbA 1c concentration increased by more than 3 times (OR = 3.69, 95% CI: 1.84–7.01, p < 0.001). Also, a rise in the dyslipidemia score, oxy score, inflammation score and DOI score by 1 unit increased the probability of higher HbA 1c concentration by 19%, 13%, 51% and 11%, respectively. In the models, after adjustment for confounding variables, endocan and DOI score remained independent predictors of HbA 1c level.

          Conclusions

          Endocan and DOI score are independently correlated with HbA 1c in patients with prediabetes and overt T2D.

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          Most cited references26

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          Endocan: A novel inflammatory indicator in cardiovascular disease?

          Endothelial dysfunction is considered as an early change in atherogenesis. Raised levels of systemic inflammatory markers are associated with cardiovascular disease (CVD). Endocan (previously known as endothelial cell specific molecule-1, ESM-1), is a potential immunoinflammatory marker that may be linked to CVD. Endocan is released by vascular endothelial cells in several organs. Endocan may play an important role in regulating cell adhesion and raised plasma levels may reflect endothelial dysfunction. Endocan levels are elevated in conditions such as chronic kidney disease, renal transplant rejection, tumor progression and hypertension. Endocan is a potential inflammatory and CVD marker. Further studies are needed to assess the relevance of endocan in clinical practice.
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            A review of the molecular mechanisms of hyperglycemia-induced free radical generation leading to oxidative stress: YARIBEYGIet al.

            The prevalence of diabetes is growing worldwide with an increasing morbidity and mortality associated with the development of diabetes complications. Free radical production is a normal biological process that is strictly controlled and has been shown to be important in normal cellular homeostasis, and in the bodies response to pathogens. However, there are several mechanisms leading to excessive free radical production that overcome the normal protective quenching mechanisms. Studies have shown that many of the diabetes complications result from excessive free radical generation and oxidative stress, and it has been shown that chronic hyperglycemia is a potent inducer for free radical production, generated through several pathways and triggering multiple molecular mechanisms. An understanding of these processes may help us to improving our preventive or therapeutic strategies. In this review, the major molecular pathways involved in free radical generation induced by hyperglycemia are described.
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              Central obesity, type 2 diabetes and insulin: exploring a pathway full of thorns

              The prevalence of type 2 diabetes (T2D) is rapidly increasing. This is strongly related to the contemporary lifestyle changes that have resulted in increased rates of overweight individuals and obesity. Central (intra-abdominal) obesity is observed in the majority of patients with T2D. It is associated with insulin resistance, mainly at the level of skeletal muscle, adipose tissue and liver. The discovery of macrophage infiltration in the abdominal adipose tissue and the unbalanced production of adipocyte cytokines (adipokines) was an essential step towards novel research perspectives for a better understanding of the molecular mechanisms governing the development of insulin resistance. Furthermore, in an obese state, the increased cellular uptake of non-esterified fatty acids is exacerbated without any subsequent β-oxidation. This in turn contributes to the accumulation of intermediate lipid metabolites that cause defects in the insulin signaling pathway. This paper examines the possible cellular mechanisms that connect central obesity with defects in the insulin pathway. It discusses the discrepancies observed from studies organized in cell cultures, animal models and humans. Finally, it emphasizes the need for therapeutic strategies in order to achieve weight reduction in overweight and obese patients with T2D.
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                Author and article information

                Journal
                Arch Med Sci
                Arch Med Sci
                AMS
                Archives of Medical Science : AMS
                Termedia Publishing House
                1734-1922
                1896-9151
                27 August 2019
                2020
                : 16
                : 1
                : 42-50
                Affiliations
                [1 ]Center of Laboratory Diagnostics, Primary Health Care Center, Podgorica, Montenegro
                [2 ]Department of Radiology, Clinical Center of Montenegro, Podgorica, Montenegro
                [3 ]Department of Medical Biochemistry, University of Belgrade – Faculty of Pharmacy, Belgrade, Serbia
                Author notes
                Corresponding author: Aleksandra Klisic, Primary Health Care Center, Trg Nikole Kovacevica 6, 81000 Podgorica, Montenegro. Phone: +382 20 481 999. E-mail: aleksandranklisic@ 123456gmail.com
                Article
                37514
                10.5114/aoms.2019.87541
                6963142
                32051704
                b1667356-6485-4947-951f-580ff0e05681
                Copyright: © 2019 Termedia & Banach

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                : 17 May 2019
                : 12 August 2019
                Categories
                Clinical Research

                Medicine
                inflammation,diabetes,oxidative stress,glycemic control,endocan
                Medicine
                inflammation, diabetes, oxidative stress, glycemic control, endocan

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