ArticleEndocrinology2009
beta-Cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 178 citations in OpenAlex.
- Mitochondria-Endoplasmic Reticulum Crosstalk in Pancreatic β-Cell Stress: A Driver of Diabetes.Cells · 2026Review
- Perspective: Beta Cell Glucose Toxicity in Type 2 Diabetes: Nrf2 and the Endogenous Antioxidant Response.Antioxidants (Basel, Switzerland) · 2026Article
- South African Herbal Teas and Diabetes-Mediated Mitochondrial Dysfunction: Emerging Evidence and Mechanistic Insights.Journal of food science · 2026Review
- Review
- Distribution of glutathione peroxidase-1 immunoreactive cells in pancreatic islets from type 1 diabetic donors and non-diabetic donors with and without islet cell autoantibodies is variable and independent of disease.Cell and tissue research · 2025Article
- Gain of pancreatic beta cell-specific SCD1 improves glucose homeostasis by maintaining functional beta cell mass under metabolic stress.Diabetologia · 2025Article
- Exploring the key role of DNA methylation as an epigenetic modulator in oxidative stress related islet cell injury in patients with type 2 diabetes mellitus: a review.Journal of diabetes and metabolic disorders · 2024Review
- Association of Dietary Selenium Intake with Type 2 Diabetes in Middle-Aged and Older Adults in China.Nutrients · 2024Article
- Antioxidants for Early Treatment of Type 2 Diabetes in Rodents and Humans: Lost in Translation?Diabetes · 2024Review
- Pancreatic β-Cell Identity Change through the Lens of Single-Cell Omics Research.International journal of molecular sciences · 2024Review
- Article
- NRF2 is required for neonatal mouse beta cell growth by maintaining redox balance and promoting mitochondrial biogenesis and function.Diabetologia · 2024Article
- Synergistic Effect of a Flavonoid-Rich Cocoa-Carob Blend and Metformin in Preserving Pancreatic Beta Cells in Zucker Diabetic Fatty Rats.Nutrients · 2024Article
- Novel lipid mediator 7Frontiers in cell and developmental biology · 2024Article
- Novel insights into the synergistic effects of selenium nanoparticles and metformin treatment of letrozole - induced polycystic ovarian syndrome: targeting PI3K/Akt signalling pathway, redox status and mitochondrial dysfunction in ovarian tissue.Redox report : communications in free radical research · 2023Article
- β Cell Stress and Endocrine Function During T1D: What Is Next to Discover?Endocrinology · 2023Article
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- Selenium and Selenoproteins in Health.Biomolecules · 2023Review
- Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress.World journal of diabetes · 2023Review
- Nrf2 and Antioxidant Response in Animal Models of Type 2 Diabetes.International journal of molecular sciences · 2023Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic hyperglycemia causes oxidative stress, which contributes to damage in various tissues and cells, including pancreatic beta-cells. The expression levels of antioxidant enzymes in the islet are low compared with other tissues, rendering the beta-cell more susceptible to damage caused by hyperglycemia. The aim of this study was to investigate whether increasing levels of endogenous glutathione peroxidase-1 (GPx-1), specifically in beta-cells, can protect them against the adverse effects of chronic hyperglycemia and assess mechanisms that may be involved. C57BLKS/J mice overexpressing the antioxidant enzyme GPx-1 only in pancreatic beta-cells were generated. The biological effectiveness of the overexpressed GPx-1 transgene was documented when beta-cells of transgenic mice were protected from streptozotocin. The transgene was then introgressed into the beta-cells of db/db mice. Without use of hypoglycemic agents, hyperglycemia in db/db-GPx(+) mice was initially ameliorated compared with db/db-GPx(-) animals and then substantially reversed by 20 wk of age. beta-Cell volume and insulin granulation and immunostaining were greater in db/db-GPx(+) animals compared with db/db-GPx(-) animals. Importantly, the loss of intranuclear musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) that was observed in nontransgenic db/db mice was prevented by GPx-1 overexpression, making this a likely mechanism for the improved glycemic control. These studies demonstrate that enhancement of intrinsic antioxidant defenses of the beta-cell protects it against deterioration during hyperglycemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.