Evidence map›Paper›PMID 23382021›Full record

ReviewEnvironmental health and preventive medicine2013

Developmental origins of obesity and type 2 diabetes: molecular aspects and role of chemicals.

Hidekuni Inadera

Open access · goldAbstract readReview
In one paragraph

Review in Environmental health and preventive medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
18.2field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. The Developmental Origins of Irritable Bowel Syndrome: A Systematic Review and Meta-Analysis.American journal of human biology : the official journal of the Human Biology Council · 2025
    Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Fetal and neonatal dioxin exposure causes sex-specific metabolic alterations in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Anti-Obesity Effect of Chitoglucan in High-Fat-Induced Obesity Mice.International journal of environmental research and public health · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021
    Review
  16. Maternal preconception PFOS exposure of Drosophila melanogaster alters reproductive capacity, development, morphology and nutrient regulation.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021
    Article
  17. Article
  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

1 author at 1 institution in 1 country.

Hidekuni InaderaDepartment of Public Health, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan. inadera@med.u-toyama.ac.jp
University of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is a leading risk factor for impaired glucose tolerance and type 2 diabetes (T2D). Although the cause of the obesity epidemic is multi-factorial and not entirely clear, the recent acceleration in incidence is too rapid to be accounted for only by genetics, the wide availability of calorie-rich foods, and increasingly sedentary lifestyles. Accumulating data suggest that the important causes of the obesity epidemic may be related to developmental and early life environmental conditions. The concept of the developmental origins of health and disease (DOHaD) suggests that adverse influences early in development, particularly during intrauterine life, may result in permanent changes in the physiology and metabolism of the infant, which in turn result in an increased risk of non-communicable diseases in adulthood. For example, undernutrition during pregnancy and rapid postnatal weight gain are associated with obesity and T2D in the adult offspring. Moreover, increasing evidence suggests that early-life exposure to a wide range of chemicals has a significant impact on the causes of metabolic disorders. Although the underlying molecular mechanisms remain to be determined, these factors can affect epigenetic processes, such as DNA methylation, allowing the developmental environment to modulate gene transcription. The objective of this review article was to summarize recent progress in the biomedical implications of the DOHaD concept, focusing on the pathogenesis of obesity and T2D, and to discuss a future direction for preventive strategies from a public health perspective.

Indexed as

Diabetes Mellitus, Type 2Environmental ExposureEnvironmental PollutantsEpigenesis, GeneticFemaleHumansNutritional Physiological PhenomenaObesityPregnancyPrenatal Exposure Delayed EffectsRisk FactorsSteroidsStress, PhysiologicalEnvironmental PollutantsSteroids

Identifiers

PMID23382021
PMCPMC3650171
OpenAlexW1988902181

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.