ArticleThe Journal of physiology2000
Zinc-induced changes in ionic currents of clonal rat pancreatic -cells: activation of ATP-sensitive K+ channels.
Article in The Journal of physiology, 2000. 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
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
20 citing papers in PubMed, 62 citations in OpenAlex.
- Zinc Homeostasis and the Risk of Type 2 Diabetes: Complex Role of ZnT8 in Insulin and Glucagon Secretion.Current nutrition reports · 2026Review
- ZnT8 loss-of-function accelerates functional maturation of hESC-derived β cells and resists metabolic stress in diabetes.Nature communications · 2022Article
- Loss of Znt8 function in diabetes mellitus: risk or benefit?Molecular and cellular biochemistry · 2021Review
- ZIGIR, a Granule-Specific ZnCell reports · 2020Article
- Paracrine signaling in islet function and survival.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Loss of ZnT8 function protects against diabetes by enhanced insulin secretion.Nature genetics · 2019Article
- The Zinc Sensing Receptor, ZnR/GPR39, in Health and Disease.International journal of molecular sciences · 2018Review
- Functional identification of islet cell types by electrophysiological fingerprinting.Journal of the Royal Society, Interface · 2017Article
- Modelling zinc changes at the hippocampal mossy fiber synaptic cleft.Journal of computational neuroscience · 2016Article
- Zinc as Allosteric Ion Channel Modulator: Ionotropic Receptors as Metalloproteins.International journal of molecular sciences · 2016Review
- Article
- Article
- Zn(2+) induces hyperpolarization by activation of a K(+) channel and increases intracellular Ca(2+) and pH in sea urchin spermatozoa.Developmental biology · 2014Review
- Zinc and insulin in pancreatic beta-cells.Endocrine · 2014Review
- Zinc inactivates melastatin transient receptor potential 2 channels via the outer pore.The Journal of biological chemistry · 2011Article
- ATP-sensitive K+ channel mediates the zinc switch-off signal for glucagon response during glucose deprivation.Diabetes · 2010Article
- Validation of TPEN as a zinc chelator in fluorescence probing of calcium in cells with the indicator Fura-2.Journal of fluorescence · 2010Article
- Insulin crystallization depends on zinc transporter ZnT8 expression, but is not required for normal glucose homeostasis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- ABCC8 and ABCC9: ABC transporters that regulate K+ channels.Pflugers Archiv : European journal of physiology · 2007Review
- Zinc is both an intracellular and extracellular regulator of KATP channel function.The Journal of physiology · 2004Article
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
The effects of zinc (Zn2+) on excitability and ionic conductances were analysed on RINm5F insulinoma cells under whole-cell and outside-out patch-clamp recording conditions. We found that extracellular application of 10-20 microM Zn2+ induced a reversible abolition of Ca2+ action potential firing, which was accompanied by an hyperpolarisation of the resting membrane potential. Higher concentrations of Zn2+, in the tens to hundreds micromolar range, induced a reversible reduction of voltage-gated Ca2+ and, to a lesser extent, K+ currents. Low-voltage-activated Ca2+ currents were more sensitive to Zn2+ block than high voltage-activated Ca2+ currents. The Zn2+-induced hyperpolarisation arose from a dose-dependent increase in a voltage-independent K+ conductance that was pharmacologically identified as an ATP-sensitive K+ (KATP) conductance. The effect was rapid in onset, readily reversible, voltage independent, and related to intracellular ATP concentration. In the presence of 1 mM intracellular ATP, half-maximal activation of KATP channels was obtained with extracellular application of 1.7 microM Zn2+. Single channel analysis revealed that extracellular Zn2+ increased the KATP channel open-state probability with no change in the single channel conductance. Our data support the hypothesis that Zn2+ binding to KATP protein subunits results in an activation of the channels, therefore regulating the resting membrane potential and decreasing the excitability of RINm5F cells. Taken together, our results suggest that Zn2+ can influence insulin secretion in pancreatic beta-cells through a negative feedback loop, involving both KATP and voltage-gated conductances.
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.