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      Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus

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          Abstract

          Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disorder characterized by chronic hyperglycemia and an inadequate response to circulatory insulin by peripheral tissues resulting in insulin resistance. Insulin resistance has a complex pathophysiology, and it is contributed to by multiple factors including oxidative stress. Oxidative stress refers to an imbalance between free radical production and the antioxidant system leading to a reduction of peripheral insulin sensitivity and contributing to the development of T2DM via several molecular mechanisms. In this review, we present the molecular mechanisms by which the oxidative milieu contributes to the pathophysiology of insulin resistance and diabetes mellitus.

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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.
          Article 0 comments Cited 522 times – based on 0 reviews     Review now
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            The global economic burden of diabetes in adults aged 20-79 years: a cost-of-illness study.

            Christian Bommer, Esther Heesemann, Vera Sagalova … (2017)
            Differences in methods and data used in past studies have limited comparisons of the cost of illness of diabetes across countries. We estimate the full global economic burden of diabetes in adults aged 20-79 years in 2015, using a unified framework across all countries. Our objective was to highlight patterns of diabetes-associated costs as well as to identify the need for further research in low-income regions.
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              Role of mitochondrial ROS in the brain: from physiology to neurodegeneration.

              Plamena Angelova, Andrey Y. Abramov (2018)
              Mitochondria are key cell organelles in that they are responsible for energy production and control many processes from signalling to cell death. The function of the mitochondrial electron transport chain is coupled with the production of reactive oxygen species (ROS) in the form of superoxide anion or hydrogen peroxide. As a result of the constant production of ROS, mitochondria are protected by highly efficient antioxidant systems. The rapidly changing levels of ROS in mitochondria, coupled with multiple essential cellular functions, make ROS apt for physiological signalling. Thus, mutations, environmental toxins and chronic ischaemic conditions could affect the mitochondrial redox balance and lead to the development of pathology. In long-living and non-mitotic cells such as neurons, oxidative stress induced by overproduction of mitochondrial ROS or impairment of the antioxidant defence results in a dysfunction of mitochondria and initiation of the cell death cascade. Mitochondrial ROS overproduction and changes in mitochondrial redox homeostasis have been shown to be involved in both a number of neurological conditions and a majority of neurodegenerative diseases. Here, we summarise the involvement of mitochondrial ROS in the mechanism of neuronal loss of major neurodegenerative disorders.
              Article 0 comments Cited 240 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Habib Yaribeygi:
                ORCID: https://orcid.org/0000-0002-1706-6212
                Amirhossein Sahebkar:
                ORCID: https://orcid.org/0000-0002-8656-1444
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2020
                Publication date (Electronic): 9 March 2020
                Volume: 2020
                Electronic Location Identifier: 8609213
                Affiliations
                1Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran
                2Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull HU3 2JZ, UK
                3Weill Cornell Medicine Qatar, Doha, Qatar
                4Halal Research Center of IRI, FDA, Tehran, Iran
                5Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
                6Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
                Author notes

                Academic Editor: Carlo G. Tocchetti

                Author information
                https://orcid.org/0000-0002-1706-6212
                https://orcid.org/0000-0002-5887-7257
                https://orcid.org/0000-0002-8656-1444
                Article
                DOI: 10.1155/2020/8609213
                PMC ID: 7085395
                PubMed ID: 32215179
                SO-VID: f0272a6b-45fa-4b7b-ba11-3a17054a8a02
                Copyright © Copyright © 2020 Habib Yaribeygi et al.
                License:

                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.

                History
                Date received : 2 November 2019
                Date revision received : 7 December 2019
                Date accepted : 4 February 2020
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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