Evidence map›Paper›PMID 30110175›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2018

Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero.

Ramkumar Mohan, Daniel Baumann, Emilyn Uy Alejandro

Abstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

37 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Developmental perfluorooctanesulfonic acid exposure impairs exocrine pancreas function in zebrafish (Danio rerio).Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Fetal Hypoglycemia Induced by PlacentalInternational journal of molecular sciences · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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.

Ramkumar MohanDepartment of Integrative Biology and Physiology, University of Minnesota , Minneapolis, Minnesota.
Daniel BaumannDepartment of Integrative Biology and Physiology, University of Minnesota , Minneapolis, Minnesota.
Emilyn Uy AlejandroDepartment of Integrative Biology and Physiology, University of Minnesota , Minneapolis, Minnesota.ORCID 0000-0002-7941-8439

Funding

O-linked-N-acetylglucosamine Post-translational Modification in Pancreatic Beta-cells Regulating ER Stress and Mitochondrial FunctionR21DK112144 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2017 to 2019
$576k
Mechanisms of Developmental Programing of beta-cell Susceptibility to GlucolipotoxicityK01DK103823 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2014 to 2017
$572k
Role of placental nutrient-sensor protein mTOR on fetal programming of beta-cell dysfunction and susceptibility to type 2 diabetesR03DK114465 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2019
$360k
NIDDK NIH HHS K01 DK103823NIDDK NIH HHS R03 DK114465NIDDK NIH HHS R21 DK112144
6 · The paper itself

Abstract

The prevalence of obesity and type 2 (T2D) diabetes is a major health concern in the United States and around the world. T2D is a complex disease characterized by pancreatic β-cell failure in association with obesity and insulin resistance in peripheral tissues. Although several genes associated with T2D have been identified, it is speculated that genetic variants account for only <10% of the risk for this disease. A strong body of data from both human epidemiological and animal studies shows that fetal nutrient factors in utero confer significant susceptibility to T2D. Numerous studies done in animals have shown that suboptimal maternal environment or placental insufficiency causes intrauterine growth restriction (IUGR) in the fetus, a critical factor known to predispose offspring to obesity and T2D, in part by causing permanent consequences in total functional β-cell mass. This review will focus on the potential contribution of the placenta in fetal programming of obesity and TD and its likely impact on pancreatic β-cell development and growth.

Indexed as

AnimalsFemaleFetal DevelopmentFetal Growth RetardationFetusHumansInsulin-Secreting CellsPlacentaPlacental InsufficiencyPregnancydiabetesfetal programminginsulin secretionisletIUGR

Identifiers

PMID30110175
PMCPMC6295492

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.