Evidence map›Paper›PMID 25437377›Full record

ArticleIslets2014

Chromanol 293B, an inhibitor of KCNQ1 channels, enhances glucose-stimulated insulin secretion and increases glucagon-like peptide-1 level in mice.

Lijie Liu, Fanfan Wang, Haiying Lu, Xiaomei Ren, Jihong Zou

Open access · bronzeAbstract read
In one paragraph

Article in Islets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Associations ofJournal of diabetes research · 2020
    Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021
    Review
  13. Review
  14. Pharmacogenetics of Type 2 Diabetes-Progress and Prospects.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors at 4 institutions in 3 countries.

Lijie Liua Department of Physiology ; Medical College of Southeast University ; Nanjing , China.
Fanfan Wang
Haiying Lu
Xiaomei Ren
Jihong Zou
Southeast University · CNInstitute of Life Sciences · INSoutheast University · BDZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-stimulated insulin secretion (GSIS) is a highly regulated process involving complex interaction of multiple factors. Potassium voltage-gated channel subfamily KQT member 1 (KCNQ1) is a susceptibility gene for type 2 diabetes (T2D) and the risk alleles of the KCNQ1 gene appear to be associated with impaired insulin secretion. The role of KCNQ1 channel in insulin secretion has been explored by previous work in clonal pancreatic β-cells but has yet to be investigated in the context of primary islets as well as intact animals. Genetic studies suggest that altered incretin glucagon-like peptide-1 (GLP-1) secretion might be a potential link between KCNQ1 variants and impaired insulin secretion, but this hypothesis has not been verified so far. In the current study, we examined KCNQ1 expression in pancreas and intestine from normal mice and then investigated the effects of chromanol 293B, a KCNQ1 channel inhibitor, on insulin secretion in vitro and in vivo. By double-immunofluorescence staining, KCNQ1 was detected in insulin-positive β-cells and GLP-1-positive L-cells. Administration of chromanol 293B enhanced GSIS in cultured islets and intact animals. Along with the potentiated insulin secretion during oral glucose tolerance tests (OGTT), plasma GLP-1 level after gastric glucose load was increased in 293B treated mice. These data not only provided new evidence for the participation of KCNQ1 in GSIS at the level of pancreatic islet and intact animal but also indicated the potential linking role of GLP-1 between KCNQ1 and insulin secretion.

Indexed as

AnimalsChromansFluorescent Antibody TechniqueGlucagon-Like Peptide 1GlucoseGlucose Tolerance TestInsulinInsulin ResistanceInsulin SecretionIntestinesIn Vitro TechniquesIslets of LangerhansKCNQ1 Potassium ChannelMicePancreasSulfonamides6-cyano-4-(N-ethylsulfonyl-N-methylamino)-3-hydroxy-2,2-dimethylchromaneChromansGlucagon-Like Peptide 1GlucoseInsulinKCNQ1 Potassium ChannelSulfonamidesAUC, Area under the curvechromanol 293BDMSO, Dimethyl sulfoxideGLP-1GLP-1, Glucagon-like peptide-1GSISGSIS, Glucose-stimulated insulin secretionGTT, Glucose tolerance testGWAS, Genome wide association studiesIPGTTislets of LangerhansITTITT, Insulin tolerance testIVGTT, Intravenous glucose tolerance testsKCNQ1KCNQ1, Potassium voltage-gated channel subfamily KQT member 1KRBH, Krebs-Ringer bicarbonate HEPES bufferOCT, Optimal Cutting Temperature CompoundOGTTOGTT, Oral glucose tolerance testsSNPs, Single nucleotide polymorphismsT2D, Type 2 diabetes

Identifiers

PMID25437377
PMCPMC4588556
OpenAlexW2031751422

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.