Evidence map›Paper›PMID 12830383›Full record

ReviewDiabetologia2003

Voltage-dependent K(+) channels in pancreatic beta cells: role, regulation and potential as therapeutic targets.

P E MacDonald, M B Wheeler

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
10.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 266 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

P E MacDonaldDepartment of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada. p.macdonald@utoronto.ca
M B Wheeler
Canada Research Chairs · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin secretion from pancreatic islet beta cells is acutely regulated by a complex interplay of metabolic and electrogenic events. The electrogenic mechanism regulating insulin secretion from beta cells is commonly referred to as the ATP-sensitive K(+) (K(ATP)) channel dependent pathway. Briefly, an increase in ATP and, perhaps more importantly, a decrease in ADP stimulated by glucose metabolism depolarises the beta cell by closing K(ATP) channels. Membrane depolarisation results in the opening of voltage-dependent Ca(2+) channels, and influx of Ca(2+) is the main trigger for insulin secretion. Repolarisation of pancreatic beta cell action potential is mediated by the activation of voltage-dependent K(+) (Kv) channels. Various Kv channel homologues have been detected in insulin secreting cells, and recent studies have shown a role for specific Kv channels as modulators of insulin secretion. Here we review the evidence supporting a role for Kv channels in the regulation of insulin secretion and discuss the potential and the limitations for beta-cell Kv channels as therapeutic targets. Furthermore, we review recent investigations of mechanisms regulating Kv channels in beta cells, which suggest that Kv channels are active participants in the regulation of beta-cell electrical activity and insulin secretion.

Indexed as

Potassium Channels, Voltage-GatedAdenosine DiphosphateAdenosine TriphosphateAnimalsDelayed Rectifier Potassium ChannelsGlucoseHumansInsulinInsulin SecretionIslets of LangerhansModels, BiologicalPotassium ChannelsPotassium Channels, Inwardly RectifyingProtein ConformationProtein SubunitsAdenosine DiphosphateAdenosine TriphosphateDelayed Rectifier Potassium ChannelsGlucoseInsulinPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassium Channels, Voltage-GatedProtein Subunits

Identifiers

PMID12830383
OpenAlexW2016688369

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.