Evidence map›Paper›PMID 27155872›Full record

ReviewDiabetologia2016

Islet biology, the CDKN2A/B locus and type 2 diabetes risk.

Yahui Kong, Rohit B Sharma, Benjamin U Nwosu, Laura C Alonso

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Review
  7. Review
  8. Prognostic value ofInternational journal of cardiology. Cardiovascular risk and prevention · 2025
    Article
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  19. ANRIL: A Long Noncoding RNA in Age-related Diseases.Mini reviews in medicinal chemistry · 2024
    Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Yahui KongAS7-2047, Division of Diabetes, Department of Medicine, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA, 01605, USA.
Rohit B SharmaAS7-2047, Division of Diabetes, Department of Medicine, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA, 01605, USA.
Benjamin U NwosuDivision of Endocrinology, Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA, USA.
Laura C AlonsoAS7-2047, Division of Diabetes, Department of Medicine, University of Massachusetts Medical School, 368 Plantation Street, Worcester, MA, 01605, USA. Laura.Alonso@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Free Fatty Acids, p16 and Pancreatic Beta Cell ProliferationR01DK095140 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ALONSO, LAURA C · 2012 to 2016
$1.9M
NIDDK NIH HHS R01 DK095140
6 · The paper itself

Abstract

Type 2 diabetes, fuelled by the obesity epidemic, is an escalating worldwide cause of personal hardship and public cost. Diabetes incidence increases with age, and many studies link the classic senescence and ageing protein p16(INK4A) to diabetes pathophysiology via pancreatic islet biology. Genome-wide association studies (GWASs) have unequivocally linked the CDKN2A/B locus, which encodes p16 inhibitor of cyclin-dependent kinase (p16(INK4A)) and three other gene products, p14 alternate reading frame (p14(ARF)), p15(INK4B) and antisense non-coding RNA in the INK4 locus (ANRIL), with human diabetes risk. However, the mechanism by which the CDKN2A/B locus influences diabetes risk remains uncertain. Here, we weigh the evidence that CDKN2A/B polymorphisms impact metabolic health via islet biology vs effects in other tissues. Structured in a bedside-to-bench-to-bedside approach, we begin with a summary of the evidence that the CDKN2A/B locus impacts diabetes risk and a brief review of the basic biology of CDKN2A/B gene products. The main emphasis of this work is an in-depth look at the nuanced roles that CDKN2A/B gene products and related proteins play in the regulation of beta cell mass, proliferation and insulin secretory function, as well as roles in other metabolic tissues. We finish with a synthesis of basic biology and clinical observations, incorporating human physiology data. We conclude that it is likely that the CDKN2A/B locus influences diabetes risk through both islet and non-islet mechanisms.

Indexed as

AnimalsCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Diabetes Mellitus, Type 2Genome-Wide Association StudyHumansIslets of LangerhansRisk FactorsCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16AgeingANRILBeta cell massCdkn2ACdkn2BCDKN2B-ASInsulin secretionOncogenep14p14ARFp15p15INK4Bp16p16INK4APancreatic beta cellProliferationReviewSenescenceTumour suppressor

Identifiers

PMID27155872
PMCPMC4930689
OpenAlexW2347147985

What OpenQuestion holds

Textmetadata
LicenceTDM
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.