Evidence map›Paper›PMID 24986330›Full record

ArticleTrends in endocrinology and metabolism: TEM2014

The pancreatic β cell: recent insights from human genetics.

Soren K Thomsen, Anna L Gloyn

Open access · hybridAbstract read
In one paragraph

Article in Trends in endocrinology and metabolism: TEM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Maturity-onset diabetes of the young (MODY): current perspectives on diagnosis and treatment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
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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 2 institutions in 1 country.

Soren K ThomsenOxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Headington, OX3 7LE, UK.
Anna L GloynOxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Headington, OX3 7LE, UK; Oxford National Institute for Health Research (NIHR) Biomedical Research Centre, Churchill Hospital, Headington, OX3 7LE, UK. Electronic address: anna.gloyn@drl.ox.ac.uk.
Oxford Centre for Diabetes, Endocrinology and Metabolism · GBUniversity of Oxford · GB

Funding

Wellcome Trust 095101
6 · The paper itself

Abstract

Diabetes mellitus is a metabolic disease characterised by relative or absolute pancreatic β cell dysfunction. Genetic variants implicated in disease risk can be identified by studying affected individuals. To understand the mechanisms driving genetic associations, variants must be translated through causative transcripts to biological insights. Studies into the genetic basis of Mendelian forms of diabetes have successfully identified genes involved in both β cell function and pancreatic development. For type 2 diabetes (T2D), genome-wide association studies (GWASs) are uncovering an ever-increasing number of susceptibility variants that exert their effect through β cell dysfunction, but translation to mechanistic understanding has in most cases been slow. Improved annotations of the islet genome and advances in whole-genome and -exome sequencing (WHS and WES) have facilitated recent progress.

Indexed as

Genetic VariationDiabetes Mellitus, Type 2Genome-Wide Association StudyGenotypeHumansInsulin-Secreting CellsdiabetesGWAShuman geneticspancreatic β cell

Identifiers

PMID24986330
PMCPMC4229643
OpenAlexW1984003932

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.