ArticleThe Journal of clinical investigation2009
Suppression of KATP channel activity protects murine pancreatic beta cells against oxidative stress.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Expression levels of KWorld journal of experimental medicine · 2024Article
- Radical oxygen species: an important breakthrough point for botanical drugs to regulate oxidative stress and treat the disorder of glycolipid metabolism.Frontiers in pharmacology · 2023Review
- Oxidative stress: The nexus of obesity and cognitive dysfunction in diabetes.Frontiers in endocrinology · 2023Review
- The Role of ABC Transporters in Skin Cells Exposed to UV Radiation.International journal of molecular sciences · 2022Review
- ATP-Sensitive Potassium Channels in Migraine: Translational Findings and Therapeutic Potential.Cells · 2022Review
- Oxidative stress and impaired insulin secretion in cystic fibrosis pig pancreas.Advances in redox research · 2022Article
- The Pancreatic ß-cell Response to Secretory Demands and Adaption to Stress.Endocrinology · 2021Review
- Relationship between Oxidative Stress and Imatinib Resistance in Model Chronic Myeloid Leukemia Cells.Biomolecules · 2021Article
- A novel palmitic acid hydroxy stearic acid (5-PAHSA) plays a neuroprotective role by inhibiting phosphorylation of the m-TOR-ULK1 pathway and regulating autophagy.CNS neuroscience & therapeutics · 2021Article
- Metformin Preserves β-Cell Compensation in Insulin Secretion and Mass Expansion in Prediabetic Nile Rats.International journal of molecular sciences · 2021Article
- Nrf2: The Master and Captain of Beta Cell Fate.Trends in endocrinology and metabolism: TEM · 2021Review
- Autocrine C-peptide protects INS1 β cells against palmitic acid-induced oxidative stress in peroxisomes by inducing catalase.Endocrinology, diabetes & metabolism · 2020Article
- Article
- Possible New Strategies for the Treatment of Congenital Hyperinsulinism.Frontiers in endocrinology · 2020Article
- Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020Review
- The role of membrane excitability in pancreatic β-cell glucotoxicity.Scientific reports · 2019Article
- ATP mediates a negative autocrine signal on stimulus-secretion coupling in mouse pancreatic β-cells.Endocrine · 2019Article
- aThe characteristics of glucose metabolism in the sulfonylurea receptor 1 knockout rat model.Molecular medicine (Cambridge, Mass.) · 2019Article
- Energy depletion and not ROS formation is a crucial step of glucolipotoxicity (GLTx) in pancreatic beta cells.Pflugers Archiv : European journal of physiology · 2018Article
- Mitochondrial KATP Channels Control Glioma Radioresistance by Regulating ROS-Induced ERK Activation.Molecular neurobiology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The enhanced oxidative stress associated with type 2 diabetes mellitus contributes to disease pathogenesis. We previously identified plasma membrane-associated ATP-sensitive K+ (KATP) channels of pancreatic beta cells as targets for oxidants. Here, we examined the effects of genetic and pharmacologic ablation of KATP channels on loss of mouse beta cell function and viability following oxidative stress. Using mice lacking the sulfonylurea receptor type 1 (Sur1) subunit of KATP channels, we found that, compared with insulin secretion by WT islets, insulin secretion by Sur1-/- islets was less susceptible to oxidative stress induced by the oxidant H2O2. This was likely, at least in part, a result of the reduced ability of H2O2 to hyperpolarize plasma membrane potential and reduce cytosolic free Ca2+ concentration ([Ca2+]c) in the Sur1-/- beta cells. Remarkably, Sur1-/- beta cells were less prone to apoptosis induced by H2O2 or an NO donor than WT beta cells, despite an enhanced basal rate of apoptosis. This protective effect was attributed to upregulation of the antioxidant enzymes SOD, glutathione peroxidase, and catalase. Upregulation of antioxidant enzymes and reduced sensitivity of Sur1-/- cells to H2O2-induced apoptosis were mimicked by treatment with the sulfonylureas tolbutamide and gliclazide. Enzyme upregulation and protection against oxidant-induced apoptosis were abrogated by agents lowering [Ca2+]c. Sur1-/- mice were less susceptible than WT mice to streptozotocin-induced beta cell destruction and subsequent hyperglycemia and death, which suggests that loss of KATP channel activity may protect against streptozotocin-induced diabetes in vivo.
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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 Socratic graph.