ArticlePloS one2012
Reactive oxygen species stimulate insulin secretion in rat pancreatic islets: studies using mono-oleoyl-glycerol.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed, 70 citations in OpenAlex.
- Nutrient and non-nutrient regulators of insulin secretion.Nature reviews. Endocrinology · 2026Review
- Hyperinsulinaemia as a cause of obesity and cardiometabolic diseases.Nature reviews. Endocrinology · 2026Review
- Tissue-specific roles of monoacylglycerol (MAG) in metabolic diseases.Immunometabolism (Cobham, Surrey) · 2026Review
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Expression, localization and regulation of NADPH oxidases in pancreatic beta cells.Redox report : communications in free radical research · 2025Article
- Mitochondrial Physiology of Cellular Redox Regulations.Physiological research · 2024Review
- Aging and "Age-Related" Diseases - What Is the Relation?Aging and disease · 2024Review
- Overnutrition, Hyperinsulinemia and Ectopic Fat: It Is Time for A Paradigm Shift in the Management of Type 2 Diabetes.International journal of molecular sciences · 2024Review
- Obesogens: a unifying theory for the global rise in obesity.International journal of obesity (2005) · 2024Review
- Reactive oxygen species: role in obesity and mitochondrial energy efficiency.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Antimicrobial protein REG3A regulates glucose homeostasis and insulin resistance in obese diabetic mice.Communications biology · 2023Article
- Information on food additives on food labels in Brazil: a critical analysis.Revista de saude publica · 2023Article
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- Pathogenesis of (smoking-related) non-communicable diseases-Evidence for a common underlying pathophysiological pattern.Frontiers in physiology · 2022Review
- Hyperinsulinemia and Its Pivotal Role in Aging, Obesity, Type 2 Diabetes, Cardiovascular Disease and Cancer.International journal of molecular sciences · 2021Review
- NADPH Oxidase (NOX) Targeting in Diabetes: A Special Emphasis on Pancreatic β-Cell Dysfunction.Cells · 2021Review
- The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021Review
- Proinflammatory Cytokines Perturb Mouse and Human Pancreatic Islet Circadian Rhythmicity and Induce Uncoordinated β-Cell Clock Gene Expression via Nitric Oxide, Lysine Deacetylases, and Immunoproteasomal Activity.International journal of molecular sciences · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Chronic exposure (24-72 hrs) of pancreatic islets to elevated glucose and fatty acid leads to glucolipoxicity characterized by basal insulin hypersecretion and impaired glucose-stimulated insulin secretion (GSIS). Our aim was to determine the mechanism for basal hypersecretion of insulin. We used mono-oleoyl-glycerol (MOG) as a tool to rapidly increase lipids in isolated rat pancreatic ß-cells and in the clonal pancreatic ß-cell line INS-1 832/13. MOG (25-400 µM) stimulated basal insulin secretion from ß-cells in a concentration dependent manner without increasing intracellular Ca(2+) or O(2) consumption. Like GSIS, MOG increased NAD(P)H and reactive oxygen species (ROS). The mitochondrial reductant ß-hydroxybutyrate (ß-OHB) also increased the redox state and ROS production, while ROS scavengers abrogated secretion. Diazoxide (0.4 mM) did not prevent the stimulatory effect of MOG, confirming that the effect was independent of the K(ATP)-dependent pathway of secretion. MOG was metabolized to glycerol and long-chain acyl-CoA (LC-CoA), whereas, acute oleate did not similarly increase LC-CoA. Inhibition of diacylglycerol kinase (DGK) did not mimic the effect of MOG on insulin secretion, indicating that MOG did not act primarily by inhibiting DGK. Inhibition of acyl-CoA synthetase (ACS) reduced the stimulatory effect of MOG on basal insulin secretion by 30% indicating a role for LC-CoA. These data suggest that basal insulin secretion is stimulated by increased ROS production, due to an increase in the mitochondrial redox state independent of the established components of GSIS.
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Registered trials
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