ArticleJournal of diabetes research2016
Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs.
Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Protective effects of Tinospora crispa and Tinospora cordifolia extracts against methylglyoxal-induced oxidative stress and apoptosis in hFOB 1.19 cells: ELISA-based evaluation and molecular docking insights with antioxidant enzymes.BMC complementary medicine and therapies · 2026Article
- Targeting Glyoxalase-1 Pathway with Natural Compounds: A Translational Strategy to Reduce Dicarbonyl Stress and Prevent Chronic Diseases.Life (Basel, Switzerland) · 2026Review
- A Comprehensive Review of Metabolic Dysfunction-Associated Steatotic Liver Disease: Its Mechanistic Development Focusing on Methylglyoxal and Counterbalancing Treatment Strategies.International journal of molecular sciences · 2025Review
- Maternal AGE Precursors During Lactation Alters Offspring Glycemic Homeostasis Early in Life.Biology · 2025Article
- Mitochondrial uncoupling protein 2: a central player in pancreatic disease pathophysiology.Molecular medicine (Cambridge, Mass.) · 2024Review
- Type 2 diabetic mellitus related osteoporosis: focusing on ferroptosis.Journal of translational medicine · 2024Review
- Molecular Assessment of Methylglyoxal-Induced Toxicity and Therapeutic Approaches in Various Diseases: Exploring the Interplay with the Glyoxalase System.Life (Basel, Switzerland) · 2024Review
- Methylglyoxal in Cardiometabolic Disorders: Routes Leading to Pathology Counterbalanced by Treatment Strategies.Molecules (Basel, Switzerland) · 2023Review
- Phenolic Acids Rescue Iron-Induced Damage in Murine Pancreatic Cells and Tissues.Molecules (Basel, Switzerland) · 2023Article
- Uncoupling protein 2 and aldolase B impact insulin release by modulating mitochondrial function and CaiScience · 2022Article
- Glyoxalase 1 knockdown induces age-related β-cell dysfunction and glucose intolerance in mice.EMBO reports · 2022Article
- Nrf2 Regulates β-Cell Mass by Suppressing β-Cell Death and Promoting β-Cell Proliferation.Diabetes · 2022Article
- Regulation of endothelial progenitor cell functions during hyperglycemia: new therapeutic targets in diabetic wound healing.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities-A Review.International journal of molecular sciences · 2021Review
- From diabetes to renal aging: the therapeutic potential of adiponectin.Journal of physiology and biochemistry · 2021Review
- Article
- The Isothiocyanate Sulforaphane Depends on the Nrf2/γ-GCL/GSH Axis to Prevent Mitochondrial Dysfunction in Cells Exposed to Methylglyoxal.Neurochemical research · 2021Article
- Role and mechanism of FLNa and UCP2 in the development of cervical cancer.Oncology reports · 2020Observational
- Downregulation of theAntioxidants (Basel, Switzerland) · 2020Article
- Chebulic Acid Prevents Methylglyoxal-Induced Mitochondrial Dysfunction in INS-1 Pancreatic β-Cells.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylglyoxal (MG) is a highly reactive glucose metabolic intermediate and a major precursor of advanced glycation end products. MG level is elevated in hyperglycemic disorders such as diabetes mellitus. Substantial evidence has shown that MG is involved in the pathogenesis of diabetes and diabetic complications. We investigated the impact of MG on insulin secretion by MIN6 and INS-1 cells and the potential mechanisms of this effect. Our study demonstrates that MG impaired insulin secretion by MIN6 or ISN-1 cells in a dose-dependent manner. It increased reactive oxygen species (ROS) production and apoptosis rate in MIN6 or ISN-1 cells and inhibited mitochondrial membrane potential (MMP) and ATP production. Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG. These effects of MG were attenuated by MG scavenger N-acetyl cysteine. Collectively, these data indicate that MG impairs insulin secretion of pancreatic β-cells through increasing ROS production. High levels of ROS can damage β-cells directly via JNK/P38 upregulation and through activation of UCP2 resulting in reduced MMP and ATP production, leading to β-cell dysfunction and impairment of insulin production.
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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.