Evidence map›Paper›PMID 38366195›Full record

ArticleDiabetologia2024

A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.

Natascia Vedovato, Maria V Salguero, Siri Atma W Greeley, Christine H Yu, Louis H Philipson, Frances M Ashcroft

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Association of theFrontiers in medicine · 2026
    Article
  4. Article
  5. Novel Phenotype due toEuropean journal of case reports in internal medicine · 2026
    Article
  6. 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

6 authors at 3 institutions in 2 countries.

Natascia VedovatoDepartment of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, UK.ORCID http://orcid.org/0000-0003-4462-5865
Maria V SalgueroDepartments of Medicine and Pediatrics, Section of Endocrinology Diabetes and Metabolism, University of Chicago, Chicago, IL, USA.ORCID http://orcid.org/0000-0002-7267-6603
Siri Atma W GreeleyDepartments of Medicine and Pediatrics, Section of Endocrinology Diabetes and Metabolism, University of Chicago, Chicago, IL, USA.ORCID http://orcid.org/0000-0002-0741-3567
Christine H YuDivision of Endocrinology, Department of Pediatric Medicine, St Jude Children's Research Hospital, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-1317-5825
Louis H PhilipsonDepartments of Medicine and Pediatrics, Section of Endocrinology Diabetes and Metabolism, University of Chicago, Chicago, IL, USA.ORCID http://orcid.org/0000-0002-2208-3607
Frances M AshcroftDepartment of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, UK. frances.ashcroft@dpag.ox.ac.uk.ORCID http://orcid.org/0000-0002-6970-1767
University of Chicago · USUniversity of Oxford · GBSt. Jude Children's Research Hospital · US

Funding

Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI RONALD N COHEN · 2013 to 2026
$20.9M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
CLINICAL THERAPEUTICST32GM007019 · NIGMS · UNIVERSITY OF CHICAGO · PI Peter Hugh O'Donnell, MARK J RATAIN · 1985 to 2026
$8.7M
Monogenic Diabetes: Next Generation Diagnosis, Treatment and ComplicationsR01DK104942 · NIDDK · UNIVERSITY OF CHICAGO · PI GREELEY, SIRI ATMA W., PHILIPSON, LOUIS H. · 2016 to 2024
$4.7M
Incretin Regulation of Insulin Secretion in Human Neonatal DiabetesK23DK094866 · NIDDK · UNIVERSITY OF CHICAGO · PI GREELEY, SIRI ATMA W. · 2012 to 2014
$515k
Biotechnology and Biological Sciences Research Council BB/R002517/1Biotechnology and Biological Sciences Research Council BB/R017220/1Medical Research Council MR/T002107/1NCATS NIH HHS UL1 TR000430NIDDK NIH HHS K23 DK094866NIDDK NIH HHS P30 DK020595NIDDK NIH HHS R01 DK104942NIGMS NIH HHS T32 GM007019
6 · The paper itself

Abstract

aims/hypothesisThe ATP-sensitive potassium (K

methodsA 31-year-old woman was diagnosed with mild hyperglycaemia during an employee screen. After three pregnancies, during which she was diagnosed with gestational diabetes, the patient continued to show elevated blood glucose and was treated with glibenclamide (known as glyburide in the USA and Canada) and metformin. Genetic testing identified a heterozygous mutation (S118L) in the KCNJ11 gene. Neither parent was known to have diabetes. We investigated the functional properties and membrane trafficking of mutant and wild-type K

resultsFunctional analysis showed no changes in the ATP sensitivity or metabolic regulation of the mutant channel. However, the Kir6.2-S118L mutation impaired surface expression of the K CONCLUSIONS/

interpretationOur data support the increasing evidence that individuals with mild loss-of-function K

Indexed as

Congenital HyperinsulinismDiabetes, GestationalPotassium Channels, Inwardly RectifyingAdenosine TriphosphateAdultFemaleGlyburideHumansInfant, NewbornMiddle AgedMutationPregnancySulfonylurea CompoundsSulfonylurea ReceptorsAdenosine TriphosphateGlyburidePotassium Channels, Inwardly RectifyingSulfonylurea CompoundsSulfonylurea ReceptorsCongenital hyperinsulinismGlibenclamideKATP channelPharmacological chaperone

Identifiers

PMID38366195
PMCPMC10954967
OpenAlexW4393056843

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.