Evidence map›Paper›PMID 26723529›Full record

ArticleMolecular and cellular endocrinology2016

Role of placental insufficiency and intrauterine growth restriction on the activation of fetal hepatic glucose production.

Stephanie R Wesolowski, William W Hay

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Article
  2. Article
  3. Fetal nutrient flux and oxidative metabolism during hypoxia: adaptive responses to defend fetal growth.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Fetal Hypoglycemia Induced by PlacentalInternational journal of molecular sciences · 2024
    Article
  9. Article
  10. Article
  11. Why is human uterine artery blood flow during pregnancy so high?American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

2 authors.

Stephanie R WesolowskiPerinatal Research Center, Department of Pediatrics, University of Colorado School of Medicine, Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: stephanie.wesolowski@ucdenver.edu.
William W HayPerinatal Research Center, Department of Pediatrics, University of Colorado School of Medicine, Colorado Anschutz Medical Campus, Aurora, CO, USA.

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI JANINE A HIGGINS · 1995 to 2026
$32.6M
Training Program in Perinatal Biology and MedicineT32HD007186 · NICHD · UNIVERSITY OF COLORADO DENVER · PI Paul Joseph Rozance · 1985 to 2026
$6.5M
TISSUE SPECIFIC REGULATION OF GLUCOSE METABOLISM AND INSULIN ACTION IN IUGR FETUSK01DK090199 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI WESOLOWSKI, STEPHANIE R · 2010 to 2014
$707k
Functional aspects of SREBP1c in intact skeletal muscleK01DK067403 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MACLEAN, PAUL S · 2005 to 2007
$397k
Effect of hypoxia on glucose metabolism in IUGR fetal liverR03DK102972 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI WESOLOWSKI, STEPHANIE R · 2014 to 2015
$155k
NICHD NIH HHS T32 HD007186NIDDK NIH HHS K01 DK090199NIDDK NIH HHS R03 DK102972
6 · The paper itself

Abstract

Glucose is the major fuel for fetal oxidative metabolism. A positive maternal-fetal glucose gradient drives glucose across the placenta and is sufficient to meet the demands of the fetus, eliminating the need for endogenous hepatic glucose production (HGP). However, fetuses with intrauterine growth restriction (IUGR) from pregnancies complicated by placental insufficiency have an early activation of HGP. Furthermore, this activated HGP is resistant to suppression by insulin. Here, we present the data demonstrating the activation of HGP in animal models, mostly fetal sheep, and human pregnancies with IUGR. We also discuss potential mechanisms and pathways that may produce and support HGP and hepatic insulin resistance in IUGR fetuses.

Indexed as

Insulin ResistanceAnimalsDisease Models, AnimalFemaleFetal Growth RetardationFetusGlucoseHumansLiverPlacental InsufficiencyPregnancySheepGlucoseFetusGlucoseInsulin resistanceIUGRLiver

Identifiers

PMID26723529
PMCPMC4921201

What Socratic holds

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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 Socratic graph.