ArticleEndocrine2015
Autocrine effect of Zn²⁺ on the glucose-stimulated insulin secretion.
Article in Endocrine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Zinc Supplementation Does Not Alter Indicators of Insulin Secretion and Sensitivity in Black and White Female Adolescents.The Journal of nutrition · 2017Trial
- Zinc Homeostasis and the Risk of Type 2 Diabetes: Complex Role of ZnT8 in Insulin and Glucagon Secretion.Current nutrition reports · 2026Review
- Replacing ZnSOAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Application of Nanoparticles: Diagnosis, Therapeutics, and Delivery of Insulin/Anti-Diabetic Drugs to Enhance the Therapeutic Efficacy of Diabetes Mellitus.Life (Basel, Switzerland) · 2022Review
- Quantitative, in situ visualization of intracellular insulin vesicles in pancreatic beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Inside the Insulin Secretory Granule.Metabolites · 2021Review
- Loss of Znt8 function in diabetes mellitus: risk or benefit?Molecular and cellular biochemistry · 2021Review
- Zinc.Advances in food and nutrition research · 2021Review
- Natural Compound α-PGG and Its Synthetic Derivative 6Cl-TGQ Alter Insulin Secretion: Evidence for Diminishing Glucose Uptake as a Mechanism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- A 3D culture platform enables development of zinc-binding prodrugs for targeted proliferation of β cells.Science advances · 2020Article
- Zinc and its regulators in pancreas.Inflammopharmacology · 2019Review
- Modeling human pancreatic beta cell dedifferentiation.Molecular metabolism · 2018Article
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Zinc status is associated with inflammation, oxidative stress, lipid, and glucose metabolism.The journal of physiological sciences : JPS · 2018Review
- The dynamic plasticity of insulin production in β-cells.Molecular metabolism · 2017Review
- Early differences in islets from prediabetic NOD mice: combined microarray and proteomic analysis.Diabetologia · 2017Article
- Analysis of Blood Concentrations of Zinc, Germanium, and Lead and Relevant Environmental Factors in a Population Sample from Shandong Province, China.International journal of environmental research and public health · 2017Article
- Zinc Transport Gets Its Zing Back: Double-Knockout of ZnT7 and ZnT8 Reveals the Importance of Zinc Transporters to Insulin Secretion.Endocrinology · 2016Article
- Lack of Association betweenJournal of diabetes research · 2016Article
- Zinc and diabetes mellitus: understanding molecular mechanisms and clinical implications.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that zinc (Zn(2+)) is required for the process of insulin biosynthesis and the maturation of insulin secretory granules in pancreatic beta (β)-cells, and that changes in Zn(2+) levels in the pancreas have been found to be associated with diabetes. Glucose-stimulation causes a rapid co-secretion of Zn(2+) and insulin with similar kinetics. However, we do not know whether Zn(2+) regulates insulin availability and secretion. Here we investigated the effect of Zn(2+) on glucose-stimulated insulin secretion (GSIS) in isolated mouse pancreatic islets. Whereas Zn(2+) alone (control) had no effect on the basal secretion of insulin, it significantly inhibited GSIS. The application of CaEDTA, by removing the secreted Zn(2+) from the extracellular milieu of the islets, resulted in significantly increased GSIS, suggesting an overall inhibitory role of secreted Zn(2+) on GSIS. The inhibitory action of Zn(2+) was mostly mediated through the activities of KATP/Ca(2+) channels. Furthermore, during brief paired-pulse glucose-stimulated Zn(2+) secretion (GSZS), Zn(2+) secretion following the second pulse was significantly attenuated, probably by the secreted endogenous Zn(2+) after the first pulse. Such an inhibition on Zn(2+) secretion following the second pulse was completely reversed by Zn(2+) chelation, suggesting a negative feedback mechanism, in which the initial glucose-stimulated Zn(2+) release inhibits subsequent Zn(2+) secretion, subsequently inhibiting insulin co-secretion as well. Taken together, these data suggest a negative feedback mechanism on GSZS and GSIS by Zn(2+) secreted from β-cells, and the co-secreted Zn(2+) may act as an autocrine inhibitory modulator.
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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.