ArticleBiochimica et biophysica acta. Bioenergetics2018
Metabolic activation-driven mitochondrial hyperpolarization predicts insulin secretion in human pancreatic beta-cells.
Article in Biochimica et biophysica acta. Bioenergetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Advanced Open-Source Experimental-Design Tools for Microplate-Based Assays with Acoustic Liquid Handling.bioRxiv : the preprint server for biology · 2026Article
- Enhancing post-thaw sperm quality in rams: quinic acid as a natural antioxidant.Frontiers in veterinary science · 2025Article
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
- Association between systemic iron status and β-cell function and insulin sensitivity in patients with newly diagnosed type 2 diabetes.Frontiers in endocrinology · 2023Article
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022Article
- β-Cell Succinate Dehydrogenase Deficiency Triggers Metabolic Dysfunction and Insulinopenic Diabetes.Diabetes · 2022Article
- ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism.Frontiers in physiology · 2022Review
- Cholesterol Sulfate Exerts Protective Effect on Pancreatic β-Cells by Regulating β-Cell Mass and Insulin Secretion.Frontiers in pharmacology · 2022Article
- Controlled power: how biology manages succinate-driven energy release.Biochemical Society transactions · 2021Article
- Review
- Review
- Mitochondrial Superoxide Production Decreases on Glucose-Stimulated Insulin Secretion in Pancreatic β Cells Due to Decreasing Mitochondrial Matrix NADH/NADAntioxidants & redox signaling · 2020Article
- Functional changes in beta cells during ageing and senescence.Diabetologia · 2020Review
- Glucose-Induced Expression of DAPIT in Pancreatic β-Cells.Biomolecules · 2020Article
- High-content fluorescence imaging with the metabolic flux assay reveals insights into mitochondrial properties and functions.Communications biology · 2020Article
- Hepcidin as a key iron regulator mediates glucotoxicity-induced pancreatic β-cell dysfunction.Endocrine connections · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Mitochondrial metabolism plays a central role in insulin secretion in pancreatic beta-cells. Generation of protonmotive force and ATP synthesis from glucose-originated pyruvate are critical steps in the canonical pathway of glucose-stimulated insulin secretion. Mitochondrial metabolism is intertwined with pathways that are thought to amplify insulin secretion with mechanisms distinct from the canonical pathway, and the relative importance of these two pathways is controversial. Here I show that glucose-induced mitochondrial membrane potential (MMP) hyperpolarization is necessary for, and predicts, the rate of insulin secretion in primary cultured human beta-cells. When glucose concentration is elevated, increased metabolism results in a substantial MMP hyperpolarization, as well as in increased rates of ATP synthesis and turnover marked by faster cell respiration. Using modular kinetic analysis I explored what properties of cellular energy metabolism enable a large glucose-induced change in MMP in human beta-cells. I found that an ATP-dependent pathway activates glucose or substrate oxidation, acting as a positive feedback in energy metabolism. This activation mechanism is essential for concomitant fast respiration and high MMP, and for a high magnitude glucose-induced MMP hyperpolarization and therefore for insulin secretion.
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Registered trials
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