ArticleThe Journal of clinical investigation2015
How do reducing equivalents increase insulin secretion?
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Exploring potential targets for natural product therapy of DN: the role of SUMOylation.Frontiers in pharmacology · 2024Review
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- Early Cytokine-Induced Transient NOX2 Activity Is ER Stress-Dependent and Impacts β-Cell Function and Survival.Antioxidants (Basel, Switzerland) · 2021Article
- Pharmacological inhibition of thioredoxin reductase increases insulin secretion and diminishes beta cell viability.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- A requirement for PAK1 to support mitochondrial function and maintain cellular redox balance via electron transport chain proteins to prevent β-cell apoptosis.Metabolism: clinical and experimental · 2021Article
- SUMO: From Bench to Bedside.Physiological reviews · 2020Review
- Insulin secretion: The nitric oxide controversy.EXCLI journal · 2020Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Glucose stimulation of insulin secretion in pancreatic β cells involves cell depolarization and subsequent opening of voltage-dependent Ca2+ channels to elicit insulin granule exocytosis. This pathway alone does not account for the entire magnitude of the secretory response in β cells. In this issue, Ferdaoussi, Dai, and colleagues reveal that insulin secretion is amplified by cytosolic isocitrate dehydrogenase-dependent transfer of reducing equivalents, which generates NADPH and reduced glutathione, which in turn activates sentrin/SUMO-specific protease-1 (SENP1). β Cell-specific deletion of Senp1 in murine models reduced the amplification of insulin exocytosis, resulting in impaired glucose tolerance. Further, their studies demonstrate that restoring intracellular NADPH or activating SENP1 improves insulin exocytosis in human β cells from donors with type 2 diabetes, suggesting a potential therapeutic target to augment 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.