Evidence map›Paper›PMID 28194805›Full record

ReviewThe Journal of physiology2017

Fetal adaptations in insulin secretion result from high catecholamines during placental insufficiency.

Sean W Limesand, Paul J Rozance

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
10.2field-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

45 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. 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
  6. IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  7. Article
  8. Review
  9. Neonatal hypoglycaemia.BMJ medicine · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Sean W LimesandSchool of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ, USA.ORCID 0000-0002-5851-0439
Paul J RozancePerinatal Research Center, University of Colorado School of Medicine, Aurora, CO, USA.
University of Arizona · USUniversity of Colorado Denver · US

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Wendy M Kohrt · 1995 to 2026
$32.6M
Prevention of Placental Insufficiency Improves Beta-Cells FunctionR01DK084842 · NIDDK · UNIVERSITY OF ARIZONA · PI SEAN W LIMESAND · 2009 to 2026
$5.6M
Nutrient Coordination of Pancreatic Vasculature and Beta-CellsR01DK088139 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI ROZANCE, PAUL JOSEPH · 2011 to 2020
$5.1M
NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK084842NIDDK NIH HHS R01 DK088139
6 · The paper itself

Abstract

Placental insufficiency and intrauterine growth restriction (IUGR) of the fetus affects approximately 8% of all pregnancies and is associated with short- and long-term disturbances in metabolism. In pregnant sheep, experimental models with a small, defective placenta that restricts delivery of nutrients and oxygen to the fetus result in IUGR. Low blood oxygen concentrations increase fetal plasma catecholamine concentrations, which lower fetal insulin concentrations. All of these observations in sheep models with placental insufficiency are consistent with cases of human IUGR. We propose that sustained high catecholamine concentrations observed in the IUGR fetus produce developmental adaptations in pancreatic β-cells that impair fetal insulin secretion. Experimental evidence supporting this hypothesis shows that chronic elevation in circulating catecholamines in IUGR fetuses persistently inhibits insulin concentrations and secretion. Elevated catecholamines also allow for maintenance of a normal fetal basal metabolic rate despite low fetal insulin and glucose concentrations while suppressing fetal growth. Importantly, a compensatory augmentation in insulin secretion occurs following inhibition or cessation of catecholamine signalling in IUGR fetuses. This finding has been replicated in normally grown sheep fetuses following a 7-day noradrenaline (norepinephrine) infusion. Together, these programmed effects will potentially create an imbalance between insulin secretion and insulin-stimulated glucose utilization in the neonate which probably explains the transient hyperinsulinism and hypoglycaemia in some IUGR infants.

Indexed as

AnimalsCatecholaminesFemaleFetal Growth RetardationFetusHumansInsulinInsulin SecretionNorepinephrinePlacental InsufficiencyPregnancyCatecholaminesInsulinNorepinephrinedevelopmental programmingepinephrineintrauterine growth restrictionnorepinephrineβ-cell

Identifiers

PMID28194805
PMCPMC5538202
OpenAlexW2588259783

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.