Cited by 654Pancreatic function and diabetesEndoplasmic Reticulum Stress and DiseaseDiabetes Treatment and Management

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The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus

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Gerber, Philipp A., Rutter, Guy A.·2017·Antioxidants & Redox Signaling

DOI 10.1089/ars.2016.6755PMC PMC5372767

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Abstract

Significance: Metabolic syndrome is a frequent precursor of type 2 diabetes mellitus (T2D), a disease that currently affects ∼8% of the adult population worldwide. Pancreatic beta-cell dysfunction and loss are central to the disease process, although understanding of the underlying molecular mechanisms is still fragmentary. Recent Advances: Oversupply of nutrients, including glucose and fatty acids, and the subsequent overstimulation of beta cells, are believed to be an important contributor to insulin secretory failure in T2D. Hypoxia has also recently been implicated in beta-cell damage. Accumulating evidence points to a role for oxidative stress in both processes. Although the production of reactive oxygen species (ROS) results from enhanced mitochondrial respiration during stimulation with glucose and other fuels, the expression of antioxidant defense genes is unusually low (or disallowed) in beta cells. Critical Issues: Not all subjects with metabolic syndrome and hyperglycemia go on to develop full-blown diabetes, implying an important role in disease risk for gene–environment interactions. Possession of common risk alleles at the SLC30A8 locus, encoding the beta-cell granule zinc transporter ZnT8, may affect cytosolic Zn 2+ concentrations and thus susceptibility to hypoxia and oxidative stress. Future Directions: Loss of normal beta-cell function, rather than total mass, is increasingly considered to be the major driver for impaired insulin secretion in diabetes. Better understanding of the role of oxidative changes, its modulation by genes involved in disease risk, and effects on beta-cell identity may facilitate the development of new therapeutic strategies to this disease. Antioxid. Redox Signal . 26, 501–518.

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Authors: Gerber, P. A., & Rutter, G. A.
Affiliations: University Hospital Zurich (CH)
Imperial College London (GB)
Corresponding author: Rutter, Guy A.
ORCID: Gerber, Philipp A.
Rutter, Guy A.
Venue: Antioxidants & Redox Signaling
Publisher: SAGE Publications
Published: 2017-04
Volume: 26
Issue: 10
Pages: 501-518
ISSN: 1523-0864 (ISSN-L)
1557-7716
DOI: 10.1089/ars.2016.6755
PMC: PMC5372767
OpenAlex: W2405977822
Cited by: 654
References: 218
Citations by year: 2026: 50 · 2025: 67 · 2024: 69 · 2023: 95 · 2022: 87 · 2021: 82 · 2020: 85 · 2019: 64 · 2018: 36 · 2017: 16
FWCI: 7.86
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Antioxidants and Redox Signaling (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
Spiral (Imperial College London) (submittedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Zurich Open Repository and Archive (University of Zurich)
Funders: Wellcome Trust (FP7/2007–2013, WT098424AIA)
European Federation of Pharmaceutical Industries and Associations (FP7/20072013)
Diabetes UK (11/0004210)
European Commission (2007–2013, FP7 2007-2013, FP7/2007)
Universitätsspital Zürich
Innovative Medicines Initiative (FP7/2007‐2013, 155005)
Directorate for Biological Sciences
Medical Research Council (MR/K001981/1, MR/J0003042/1)
Biotechnology and Biological Sciences Research Council (BB/J015873/1)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords: oxidative stress, hypoxia, beta-cell dysfunction, type 2 diabetes, insulin secretion, reactive oxygen species, mitochondrial respiration, antioxidant defense genes, metabolic syndrome, SLC30A8, zinc transporter 8, zinc, gene-environment interaction, beta-cell identity
MeSH terms: Animals, Hypoxia, Antioxidants, Diabetes Mellitus, Diabetes Mellitus, Type 2, Glucose, Humans, Insulin, Islets of Langerhans, Mitochondria, Zinc, Islets of Langerhans Transplantation, Reactive Oxygen Species, Oxidative Stress, Lipid Metabolism, Insulin-Secreting Cells

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The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus

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