ArticleDiabetologia2015
Mitochondrial succinate dehydrogenase is involved in stimulus-secretion coupling and endogenous ROS formation in murine beta cells.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 33 citations in OpenAlex.
- ROMO1 and mitochondrial complex II/SDH are required for spare respiratory capacity and glucose homeostasis in mice.Diabetologia · 2026Article
- Hepatic antioxidant capacity, immune response, and glycolysis of Tibetan sheep in response to dietary soluble protein levels.Protoplasma · 2025Article
- Succinate in innate immunity: linking metabolic reprogramming to immune modulation.Frontiers in immunology · 2025Review
- Redox Status as a Key Driver of Healthy Pancreatic Beta-Cells.Physiological research · 2024Review
- Vitamin C as Scavenger of Reactive Oxygen Species during Healing after Myocardial Infarction.International journal of molecular sciences · 2024Review
- Targeting metabolic pathways: a novel therapeutic direction for type 2 diabetes.Frontiers in cellular and infection microbiology · 2023Article
- ATP-Sensitive Potassium Channels in Migraine: Translational Findings and Therapeutic Potential.Cells · 2022Review
- β-Cell Succinate Dehydrogenase Deficiency Triggers Metabolic Dysfunction and Insulinopenic Diabetes.Diabetes · 2022Article
- Anti-aging effects of chlorpropamide depend on mitochondrial complex-II and the production of mitochondrial reactive oxygen species.Acta pharmaceutica Sinica. B · 2022Article
- Molecular docking analysis of melamine with nuclear factor erythroid 2-related factor 2 and succinate dehydrogenase.Bioinformation · 2022Article
- Review
- Mitochondrial complex II and reactive oxygen species in disease and therapy.Redox report : communications in free radical research · 2020Review
- Article
- Vildagliptin Attenuates Huntington's Disease through Activation of GLP-1 Receptor/PI3K/Akt/BDNF Pathway in 3-Nitropropionic Acid Rat Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Possible New Strategies for the Treatment of Congenital Hyperinsulinism.Frontiers in endocrinology · 2020Article
- Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes.Antioxidants & redox signaling · 2019Article
- ATP mediates a negative autocrine signal on stimulus-secretion coupling in mouse pancreatic β-cells.Endocrine · 2019Article
- Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance.Oxidative medicine and cellular longevity · 2019Article
- Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity.Molecules (Basel, Switzerland) · 2018Review
- Metabolic Alterations in a Slow-Paced Model of Pancreatic Cancer-Induced Wasting.Oxidative medicine and cellular longevity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGeneration of reduction equivalents is a prerequisite for nutrient-stimulated insulin secretion. Mitochondrial succinate dehydrogenase (SDH) fulfils a dual function with respect to mitochondrial energy supply: (1) the enzyme is part of mitochondrial respiratory chains; and (2) it catalyses oxidation of succinate to fumarate in the Krebs cycle. The aim of our study was to elucidate the significance of SDH for beta cell stimulus-secretion coupling (SSC).
methodsMitochondrial variables, reactive oxygen species (ROS) and cytosolic Ca(2+) concentration ([Ca(2+)]c) were measured by fluorescence techniques and insulin release by radioimmunoassay in islets or islet cells of C57Bl/6N mice.
resultsInhibition of SDH with 3-nitropropionic acid (3-NPA) or monoethyl fumarate (MEF) reduced glucose-stimulated insulin secretion. Inhibition of the ATP-sensitive K(+) channel (KATP channel) partly prevented this effect, whereas potentiation of antioxidant defence by superoxide dismutase mimetics (TEMPOL and mito-TEMPO) or by nuclear factor erythroid 2-related factor 2 (Nrf-2)-mediated upregulation of antioxidant enzymes (oltipraz, tert-butylhydroxyquinone) did not diminish the inhibitory influence of 3-NPA. Blocking SDH decreased glucose-stimulated increase in intracellular FADH2 concentration without alterations in NAD(P)H. In addition, 3-NPA and MEF drastically reduced glucose-induced hyperpolarisation of mitochondrial membrane potential, indicative of decreased ATP production. As a consequence, the glucose-stimulated rise in [Ca(2+)]c was significantly delayed and reduced. Acute application of 3-NPA interrupted glucose-driven oscillations of [Ca(2+)]c. 3-NPA per se did not elevate intracellular ROS, but instead prevented glucose-induced ROS accumulation. CONCLUSIONS/
interpretationSDH is an important regulator of insulin secretion and ROS production. Inhibition of SDH interrupts membrane-potential-dependent SSC, pointing to a pivotal role of mitochondrial FAD/FADH2 homeostasis for the maintenance of glycaemic control.
Indexed as
Identifiers
What OpenQuestion holds
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.