Evidence map›Paper›PMID 16133261›Full record

ArticlePflugers Archiv : European journal of physiology2005

Effects of I(Ks) channel inhibitors in insulin-secreting INS-1 cells.

Susanne Ullrich, Jiping Su, Felicia Ranta, Oliver H Wittekindt, Frederic Ris, Martin Rösler, Uwe Gerlach, Dirk Heitzmann, Richard Warth, Florian Lang

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 5 pooled it
0.6field-weighted citation impact, top 28% 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

50 citing papers in PubMed, 5 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Associations ofJournal of diabetes research · 2020
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Review
  8. Cannabidiol inhibits both human KActa pharmacologica Sinica · 2026
    Article
  9. Association betweenFrontiers in endocrinology · 2025
    Article
  10. World journal of diabetes · 2024
    Article
  11. Article
  12. Review
  13. Pharmacogenetics of new classes of antidiabetic drugs.Bosnian journal of basic medical sciences · 2021
    Review
  14. Article
  15. Review
  16. Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021
    Review
  17. Review
  18. Genetics of Obesity in East Asians.Frontiers in genetics · 2020
    Review
  19. Article
  20. Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Article
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

10 authors at 6 institutions in 3 countries.

Susanne UllrichInstitute of Neurophysiology, University of Köln, Robert Koch Strasse 39, 50931 Cologne, Germany. susanne.ullrich@uni-tuebingen.de
Jiping Su
Felicia Ranta
Oliver H Wittekindt
Frederic Ris
Martin Rösler
Uwe Gerlach
Dirk Heitzmann
Richard Warth
Florian Lang
University of Cologne · DEUniversity of Regensburg · DEUniversity of Tübingen · DELouis-Jeantet Foundation · CHSanofi (Germany) · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Potassium channels regulate insulin secretion. The closure of K(ATP) channels leads to membrane depolarisation, which triggers Ca(2+) influx and stimulates insulin secretion. The subsequent activation of K(+) channels terminates secretion. We examined whether KCNQ1 channels are expressed in pancreatic beta-cells and analysed their functional role. Using RT/PCR cellular mRNA of KCNQ1 but not of KCNE1 channels was detected in INS-1 cells. Effects of two sulfonamide analogues, 293B and HMR1556, inhibitors of KCNQ1 channels, were examined on voltage-activated outwardly rectifying K(+) currents using the patch-clamp method. It was found that 293B inhibited 60% of whole-cell outward currents induced by voltage pulses from -70 to +50 mV with a concentration for half-maximal inhibition (IC(50)) of 37 microM. The other sulfonamide analogue HMR1556 inhibited 48% of the outward current with an IC(50) of 7 microM. The chromanol 293B had no effect on tolbutamide-sensitive K(ATP) channels. Action potentials induced by current injections were broadened and after-repolarisation was attenuated by 293B. Insulin secretion in the presence but not in the absence of tolbutamide was significantly increased by 293B. These results suggest that 293B- and HMR1556-sensitive channels, probably in concert with other voltage-activated K(+) channels, influence action potential duration and frequency and thus insulin secretion.

Indexed as

4-AminopyridineAnimalsCell Line, TumorChromansGene ExpressionInsulinInsulin-Secreting CellsInsulin SecretionKCNQ1 Potassium ChannelMembrane PotentialsRatsSulfonamidesTetraethylammoniumTolbutamide4-Aminopyridine6-cyano-4-(N-ethylsulfonyl-N-methylamino)-3-hydroxy-2,2-dimethylchromaneChromansHMR 1556InsulinKCNQ1 Potassium ChannelSulfonamidesTetraethylammoniumTolbutamide

Identifiers

PMID16133261
OpenAlexW1989810385

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.