Evidence map›Paper›PMID 33833312›Full record

ArticleScientific reports2021

Autocrine IGF2 programmes β-cell plasticity under conditions of increased metabolic demand.

Ionel Sandovici, Constanze M Hammerle, Sam Virtue, Yurena Vivas-Garcia, Adriana Izquierdo-Lahuerta, Susan E Ozanne, Antonio Vidal-Puig, Gema Medina-Gómez, Miguel Constância

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

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  9. Cells · 2022
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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

9 authors at 4 institutions in 2 countries.

Ionel Sandovici *Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK. is299@cam.ac.uk.
Constanze M Hammerle *Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK. czmh@novonordisk.com.
Sam VirtueMetabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.
Yurena Vivas-GarciaÁrea de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, 28922, Alcorcón, Madrid, Spain.
Adriana Izquierdo-LahuertaÁrea de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, 28922, Alcorcón, Madrid, Spain.
Susan E OzanneMetabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.
Antonio Vidal-PuigMetabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.
Gema Medina-GómezÁrea de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, 28922, Alcorcón, Madrid, Spain.
Miguel ConstânciaMetabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK. jmasmc2@cam.ac.uk.
Universidad Rey Juan Carlos · ESWellcome/MRC Institute of Metabolic Science · GBAddenbrooke's Hospital · GBNational Institute for Health Research · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H003312/1Medical Research Council MC_UU_00014/2Medical Research Council MC_UU_00014/4Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/4Medical Research Council MC_UU_12012/5Medical Research Council MRC 979241Medical Research Council MRC_MC_UU_00014/4Medical Research Council MRC_MC_UU_12012/4Medical Research Council MRC_MC_UU_12012/5Wellcome Trust
6 · The paper itself

Abstract

When exposed to nutrient excess and insulin resistance, pancreatic β-cells undergo adaptive changes in order to maintain glucose homeostasis. The role that growth control genes, highly expressed in early pancreas development, might exert in programming β-cell plasticity in later life is a poorly studied area. The imprinted Igf2 (insulin-like growth factor 2) gene is highly transcribed during early life and has been identified in recent genome-wide association studies as a type 2 diabetes susceptibility gene in humans. Hence, here we investigate the long-term phenotypic metabolic consequences of conditional Igf2 deletion in pancreatic β-cells (Igf2

Indexed as

AnimalsCell PlasticityFemaleGlucoseHomeostasisInsulinInsulin-Like Growth Factor IIInsulin ResistanceInsulin-Secreting CellsMaleMiceMice, KnockoutPregnancyGlucoseIGF2 protein, mouseInsulinInsulin-Like Growth Factor II

Identifiers

PMID33833312
PMCPMC8032793
OpenAlexW3152041147

What OpenQuestion holds

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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.