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      Oxidative Stress Genes, Antioxidants and Coronary Artery Disease in 
Type 2 Diabetes Mellitus

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The worldwide increasing prevalence of obesity and sedentary lifestyle is the main cause of the rising incidence of T2DM. Due to chronic macrovascular and microvascular complications, T2DM represent a huge socioeconomic burden in the world. Oxidative stress is a key pathogenic mechanism implicated in diabetic coronary artery disease (CAD). Polymorphisms of oxidative stress genes are known to influence oxidative stress levels and are therefore thought to impact CAD pathogenesis. Identifying higher risk groups would be rational, since it would allow better sample selection and thus better results in antioxidant trials. In this review, we summarize the evidence of oxidative stress gene polymorphisms related to the pathogenesis of CAD. Moreover, we provide a review of antioxidants tested in subjects with CAD.

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          ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis.

          Benoit D'Autréaux, Michel B. Toledano (2007)
          Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.
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            Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future.

            Steven E. Kahn, Mark E. Cooper, Stefano Del Prato (2014)
            Glucose metabolism is normally regulated by a feedback loop including islet β cells and insulin-sensitive tissues, in which tissue sensitivity to insulin affects magnitude of β-cell response. If insulin resistance is present, β cells maintain normal glucose tolerance by increasing insulin output. Only when β cells cannot release sufficient insulin in the presence of insulin resistance do glucose concentrations rise. Although β-cell dysfunction has a clear genetic component, environmental changes play an essential part. Modern research approaches have helped to establish the important role that hexoses, aminoacids, and fatty acids have in insulin resistance and β-cell dysfunction, and the potential role of changes in the microbiome. Several new approaches for treatment have been developed, but more effective therapies to slow progressive loss of β-cell function are needed. Recent findings from clinical trials provide important information about methods to prevent and treat type 2 diabetes and some of the adverse effects of these interventions. However, additional long-term studies of drugs and bariatric surgery are needed to identify new ways to prevent and treat type 2 diabetes and thereby reduce the harmful effects of this disease. Copyright © 2014 Elsevier Ltd. All rights reserved.
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              Vitamin E consumption and the risk of coronary heart disease in men.

              E B Rimm, M Stampfer, A Ascherio … (1993)
              The oxidative modification of low-density lipoproteins increases their incorporation into the arterial intima, an essential step in atherogenesis. Although dietary antioxidants, such as vitamin C, carotene, and vitamin E, have been hypothesized to prevent coronary heart disease, prospective epidemiologic data are sparse. In 1986, 39,910 U.S. male health professionals 40 to 75 years of age who were free of diagnosed coronary heart disease, diabetes, and hypercholesterolemia completed detailed dietary questionnaires that assessed their usual intake of vitamin C, carotene, and vitamin E in addition to other nutrients. During four years of follow-up, we documented 667 cases of coronary disease. After controlling for age and several coronary risk factors, we observed a lower risk of coronary disease among men with higher intakes of vitamin E (P for trend = 0.003). For men consuming more than 60 IU per day of vitamin E, the multivariate relative risk was 0.64 (95 percent confidence interval, 0.49 to 0.83) as compared with those consuming less than 7.5 IU per day. As compared with men who did not take vitamin E supplements, men who took at least 100 IU per day for at least two years had a multivariate relative risk of coronary disease of 0.63 (95 percent confidence interval, 0.47 to 0.84). Carotene intake was not associated with a lower risk of coronary disease among those who had never smoked, but it was inversely associated with the risk among current smokers (relative risk, 0.30; 95 percent confidence interval, 0.11 to 0.82) and former smokers (relative risk, 0.60; 95 percent confidence interval, 0.38 to 0.94). In contrast, a high intake of vitamin C was not associated with a lower risk of coronary disease. These data do not prove a causal relation, but they provide evidence of an association between a high intake of vitamin E and a lower risk of coronary heart disease in men. Public policy recommendations with regard to the use of vitamin E supplements should await the results of additional studies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cardiovasc Hematol Agents Med Chem
                Journal ID (iso-abbrev): Cardiovasc Hematol Agents Med Chem
                Journal ID (publisher-id): CHAMC
                Title: Cardiovascular & Hematological Agents in Medicinal Chemistry
                Publisher: Bentham Science Publishers
                ISSN (Print): 1871-5257
                ISSN (Electronic): 1875-6182
                Publication date (Electronic): April 2016
                Publication date (Print): April 2016
                Volume: 14
                Issue: 1
                Pages: 23-38
                Affiliations
                [1 ]General Hospital Rakičan, Murska Sobota, Slovenia;
                [2 ]Institute of Histology and Embryology, Faculty of Medicine, University of Ljubljana, Slovenia
                Author notes
                [* ]Address correspondence to this author at the Institute of Histology and Embryology, Faculty of Medicine Ljubljana, University of Ljubljana, Korytkova 2, 1105 Ljubljana, Slovenia; Tel: +386 1 543 7367; Fax: + 386 1 543 7361; E-mail: daniel.petrovic@ 123456mf.uni-lj.si
                Article
                Publisher ID: CHAMC-14-23
                DOI: 10.2174/1871525714666160407143416
                PMC ID: 5425652
                PubMed ID: 27052028
                SO-VID: ceed3ac2-5746-4c3f-befe-154905a81556
                Copyright © © 2016 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 14 February 2016
                Date revision received : 21 March 2012
                Date accepted : 29 March 2016
                Categories
                Subject: Article

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: antioxidants,coronary artery disease,diabetes mellitus,insulin,obesity,oxidative stress
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: antioxidants, coronary artery disease, diabetes mellitus, insulin, obesity, oxidative stress

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