ArticleCell death & disease2019
Glutathione prevents chronic oscillating glucose intake-induced β-cell dedifferentiation and failure.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of reactive oxygen species on bone regeneration in diabetes: Mechanisms and therapeutic strategies.Redox biology · 2025Review
- Oxidative Stress, Glutathione Insufficiency, and Inflammatory Pathways in Type 2 Diabetes Mellitus: Implications for Therapeutic Interventions.Biomedicines · 2024Review
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Glutathione Induces Keap1 S-Glutathionylation and Mitigates Oscillating Glucose-Induced β-Cell Dysfunction by Activating Nrf2.Antioxidants (Basel, Switzerland) · 2024Article
- Integrating transcriptomics and metabolomics to reveal the protective effect and mechanism of Bushen Kangshuai Granules on the elderly people.Frontiers in pharmacology · 2024Article
- Review
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- Article
- Differentially Expressed Genes Regulating Glutathione Metabolism, Protein-Folding, and Unfolded Protein Response in Pancreatic β-Cells in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Article
- Molecular Genetics of Abnormal Redox Homeostasis in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Kinetic and data-driven modeling of pancreatic β-cell central carbon metabolism and insulin secretion.PLoS computational biology · 2022Article
- Randomized Clinical Trial of How Long-Term Glutathione Supplementation Offers Protection from Oxidative Damage and Improves HbA1c in Elderly Type 2 Diabetic Patients.Antioxidants (Basel, Switzerland) · 2022Article
- Glutathione prevents high glucose-induced pancreatic fibrosis by suppressing pancreatic stellate cell activation via the ROS/TGFβ/SMAD pathway.Cell death & disease · 2022Article
- The Link between Type 2 Diabetes Mellitus and the Polymorphisms of Glutathione-Metabolizing Genes Suggests a New Hypothesis Explaining Disease Initiation and Progression.Life (Basel, Switzerland) · 2021Article
- Review
- VMAT2 Safeguards β-Cells Against Dopamine Cytotoxicity Under High-Fat Diet-Induced Stress.Diabetes · 2020Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modern lifestyles have altered diet and metabolic homeostasis, with increased sugar intake, glycemic index, and prediabetes. A strong positive correlation between sugar consumption and diabetic incidence is revealed, but the underlying mechanisms remain obscure. Here we show that oral intake of long-term oscillating glucose (LOsG) (4 times/day) for 38 days, which produces physiological glycemic variability in rats, can lead to β-cells gaining metabolic memory in reactive oxygen species (ROS) stress. This stress leads to suppression of forkhead box O1 (FoxO1) signaling and subsequent upregulation of thioredoxin interacting protein, inhibition of insulin and SOD-2 expression, re-expression of Neurog3, and β-cell dedifferentiation and functional failure. LOsG-treated animals develop prediabetes exhibiting hypoinsulinemia and glucose intolerance. Dynamic and timely administration of antioxidant glutathione prevents LOsG/ROS-induced β-cell failure and prediabetes. We propose that ROS stress is the initial step in LOsG-inducing prediabetes. Manipulating glutathione-related pathways may offer novel options for preventing the occurrence and development of diabetes.
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