Evidence map›Paper›PMID 37971140›Full record

ReviewEndocrine reviews2024

Neurodevelopmental Programming of Adiposity: Contributions to Obesity Risk.

Alicja A Skowronski, Rudolph L Leibel, Charles A LeDuc

Open access · hybridAbstract readReview
In one paragraph

Review in Endocrine reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
14.5field-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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Beyond Deterministic Fetal Programming: Intrauterine Exposures and the Multifactorial Origins of Adiposity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  2. Article
  3. Article
  4. On the Intimate Relationship of Adiposity to Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Observational
  14. AgRP neurons mediate activity-dependent development of oxytocin connectivity and autonomic regulation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Review
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Alicja A SkowronskiDivision of Molecular Genetics, Department of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0003-4648-8593
Rudolph L LeibelDivision of Molecular Genetics, Department of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0002-6062-7222
Charles A LeDucDivision of Molecular Genetics, Department of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA.ORCID 0000-0002-2073-5050
Columbia University Irving Medical Center · US

Funding

RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
The molecular genetic analysis of human obesityR01DK052431 · NIDDK · ROCKEFELLER UNIVERSITY · PI CHUNG, WENDY K, LEIBEL, RUDOLPH L · 1996 to 2020
$11.6M
NIDDK NIH HHS P30 DK026687NIDDK NIH HHS R01 DK052431NIH HHS R01 DK052431
6 · The paper itself

Abstract

This review analyzes the published evidence regarding maternal factors that influence the developmental programming of long-term adiposity in humans and animals via the central nervous system (CNS). We describe the physiological outcomes of perinatal underfeeding and overfeeding and explore potential mechanisms that may mediate the impact of such exposures on the development of feeding circuits within the CNS-including the influences of metabolic hormones and epigenetic changes. The perinatal environment, reflective of maternal nutritional status, contributes to the programming of offspring adiposity. The in utero and early postnatal periods represent critically sensitive developmental windows during which the hormonal and metabolic milieu affects the maturation of the hypothalamus. Maternal hyperglycemia is associated with increased transfer of glucose to the fetus driving fetal hyperinsulinemia. Elevated fetal insulin causes increased adiposity and consequently higher fetal circulating leptin concentration. Mechanistic studies in animal models indicate important roles of leptin and insulin in central and peripheral programming of adiposity, and suggest that optimal concentrations of these hormones are critical during early life. Additionally, the environmental milieu during development may be conveyed to progeny through epigenetic marks and these can potentially be vertically transmitted to subsequent generations. Thus, nutritional and metabolic/endocrine signals during perinatal development can have lifelong (and possibly multigenerational) impacts on offspring body weight regulation.

Indexed as

LeptinPrenatal Exposure Delayed EffectsAdiposityAnimalsFemaleHumansInsulinMaternal Nutritional Physiological PhenomenaObesityPregnancyInsulinLeptinadipositydevelopmental programmingepigeneticshypothalamusobesity

Identifiers

PMID37971140
PMCPMC10911958
OpenAlexW4388736716

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.