Evidence map›Paper›PMID 23463236›Full record

ReviewCellular and molecular life sciences : CMLS2013

Developmental and environmental epigenetic programming of the endocrine pancreas: consequences for type 2 diabetes.

Ionel Sandovici, Constanze M Hammerle, Susan E Ozanne, Miguel Constância

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2013. 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
7.6field-weighted citation impact, top 2% 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, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Reduced uterine perfusion pressure causes loss of pancreatic β-cell area but normal function in fetal rat offspring.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  11. Article
  12. Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Review
  13. Article
  14. Epigenetic control of β-cell function and failure.Diabetes research and clinical practice · 2017
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  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

4 authors at 2 institutions in 1 country.

Ionel SandoviciDepartment of Obstetrics and Gynaecology, Metabolic Research Laboratories, University of Cambridge, Cambridge CB2 0SW, UK. is299@cam.ac.uk
Constanze M Hammerle
Susan E Ozanne
Miguel Constância
University of Cambridge · GBNational Institute for Health Research · GB

Funding

Biotechnology and Biological Sciences Research Council BB/D007909/1Biotechnology and Biological Sciences Research Council BB/F015364/1Biotechnology and Biological Sciences Research Council BB/H003312/1British Heart Foundation FS/09/029/27902Medical Research Council G0600717Medical Research Council MC_UU_12012/4
6 · The paper itself

Abstract

The development of the endocrine pancreas is controlled by a hierarchical network of transcriptional regulators. It is increasingly evident that this requires a tightly interconnected epigenetic "programme" to drive endocrine cell differentiation and maintain islet function. Epigenetic regulators such as DNA and histone-modifying enzymes are now known to contribute to determination of pancreatic cell lineage, maintenance of cellular differentiation states, and normal functioning of adult pancreatic endocrine cells. Persistent effects of an early suboptimal environment, known to increase risk of type 2 diabetes in later life, can alter the epigenetic control of transcriptional master regulators, such as Hnf4a and Pdx1. Recent genome-wide analyses also suggest that an altered epigenetic landscape is associated with the β cell failure observed in type 2 diabetes and aging. At the cellular level, epigenetic mechanisms may provide a mechanistic link between energy metabolism and stable patterns of gene expression. Key energy metabolites influence the activity of epigenetic regulators, which in turn alter transcription to maintain cellular homeostasis. The challenge is now to understand the detailed molecular mechanisms that underlie these diverse roles of epigenetics, and the extent to which they contribute to the pathogenesis of type 2 diabetes. In-depth understanding of the developmental and environmental epigenetic programming of the endocrine pancreas has the potential to lead to novel therapeutic approaches in diabetes.

Indexed as

Epigenesis, GeneticAnimalsDiabetes Mellitus, Type 2Gene-Environment InteractionGene Expression Regulation, DevelopmentalHumansIslets of Langerhans

Identifiers

PMID23463236
PMCPMC11113912
OpenAlexW2018796383

What OpenQuestion holds

Textmetadata
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.