Evidence map›Paper›PMID 26448950›Full record

ReviewJournal of diabetes research2015

KCNJ11: Genetic Polymorphisms and Risk of Diabetes Mellitus.

Polin Haghvirdizadeh, Zahurin Mohamed, Nor Azizan Abdullah, Pantea Haghvirdizadeh, Monir Sadat Haerian, Batoul Sadat Haerian

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Robust Mixed Model Association Test for Gene-Environment Interactions.medRxiv : the preprint server for health sciences · 2025
    Article
  7. Article
  8. Article
  9. Narra J · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. International journal of medical sciences · 2025
    Article
  14. Association ofDiabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  15. Article
  16. International journal of endocrinology · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Polin HaghvirdizadehPharmacogenomics Lab, Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.
Zahurin MohamedPharmacogenomics Lab, Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.
Nor Azizan AbdullahDepartment of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.
Pantea HaghvirdizadehDepartment of Biology, Faculty of Science, Azad University, Tehran, Iran.
Monir Sadat HaerianShahid Beheshti University of Medical Sciences, P.O. Box 19395-4763, Tehran, Iran ; Food and Drug Control Reference Labs Center (FDCRLC), Ministry of Health and Medical Education, Tehran 131456-8784, Iran.
Batoul Sadat HaerianPharmacogenomics Lab, Department of Pharmacology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.
University of Malaya · MYIslamic Azad University, Tehran · IRMinistry of Health and Medical Education · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is a major worldwide health problem and its prevalence has been rapidly increasing in the last century. It is caused by defects in insulin secretion or insulin action or both, leading to hyperglycemia. Of the various types of DM, type 2 occurs most frequently. Multiple genes and their interactions are involved in the insulin secretion pathway. Insulin secretion is mediated through the ATP-sensitive potassium (KATP) channel in pancreatic beta cells. This channel is a heteromeric protein, composed of four inward-rectifier potassium ion channel (Kir6.2) tetramers, which form the pore of the KATP channel, as well as sulfonylurea receptor 1 subunits surrounding the pore. Kir6.2 is encoded by the potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) gene, a member of the potassium channel genes. Numerous studies have reported the involvement of single nucleotide polymorphisms of the KCNJ11 gene and their interactions in the susceptibility to DM. This review discusses the current evidence for the contribution of common KCNJ11 genetic variants to the development of DM. Future studies should concentrate on understanding the exact role played by these risk variants in the development of DM.

Indexed as

Polymorphism, GeneticCell MembraneDiabetes MellitusGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansInsulinInsulin-Secreting CellsInsulin SecretionKcnj11 ChannelMutationPolymorphism, Single NucleotidePotassium Channels, Inwardly RectifyingRisk FactorsSulfonylurea ReceptorsABCC8 protein, humanInsulinKcnj11 ChannelPotassium Channels, Inwardly RectifyingSulfonylurea Receptors

Identifiers

PMID26448950
PMCPMC4584059
OpenAlexW2015290613

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.