Evidence map›Paper›PMID 23727517›Full record

ArticleAmerican journal of obstetrics and gynecology2013

Elevated glucocorticoids during ovine pregnancy increase appetite and produce glucose dysregulation and adiposity in their granddaughters in response to ad libitum feeding at 1 year of age.

Nathan M Long, Derek T Smith, Stephen P Ford, Peter W Nathanielsz

Open access · greenAbstract read
In one paragraph

Article in American journal of obstetrics and gynecology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.4field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Prenatal Steroids and Metabolic Dysfunction: Lessons from Sheep.Annual review of animal biosciences · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

4 authors at 2 institutions in 1 country.

Nathan M LongCenter for the Study of Fetal Programming, Department of Animal Science, University of Wyoming, Laramie, WY; Department of Animal and Veterinary Science, College of Agriculture, Forestry, and Life Sciences, Clemson University, Clemson, SC.
Derek T Smith
Stephen P Ford
Peter W Nathanielsz
University of Wyoming · USThe University of Texas Health Science Center at San Antonio · US

Funding

Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI LIBERLES, DAVID A. · 2001 to 2011
$28.2M
PARTURITION AND FETAL PRIMATE HYPOTHALAMIC FUNCTIONP01HD021350 · NICHD · UNIVERSITY OF WYOMING · PI NIJLAND, MARK J · 1987 to 2018
$19.9M
NCRR NIH HHS P20 RR016474NCRR NIH HHS P20-RR-16474-04NICHD NIH HHS HD 21350NICHD NIH HHS P01 HD021350
6 · The paper itself

Abstract

objectiveSynthetic glucocorticoids (sGCs) are administered to women threatening preterm labor. We have shown multigenerational endocrine and metabolic effects of fetal sGC exposure. We hypothesized that sGC exposure would alter the second filial generation (F2) offspring neonatal leptin peak that controls development of appetitive behavior with metabolic consequences. STUDY

designF0 nulliparous ewes were bred to a single ram. Beginning at day 103 of gestation (term 150 days), dexamethasone (DEX) ewes received 4 injections of 2 mg DEX intramuscularly, 12 hours apart. Control ewes received saline. Ewes lambed naturally. At 22 months of age, F1 offspring were mated to produce F2 offspring. At 10 months of age, F2 female offspring were placed on an ad libitum feeding challenge for 12 weeks.

resultsDEX F2 female offspring did not show a postnatal leptin peak and their plasma cortisol concentration was elevated in the first days of life. During the feeding challenge, DEX F2 offspring consumed 10% more feed and gained 20% more weight compared with control F2 offspring. At the end of the feeding challenge, DEX F2 offspring had greater adiposity compared with control F2 offspring. F2 sGC offspring showed impaired insulin secretion in response to an intravenous glucose tolerance test.

conclusionsGC administration to F0 mothers eliminates the neonatal leptin peak in F2 female offspring potentially by inhibition caused by elevated cortisol in the DEX F2 offspring. F2 offspring showed increased appetite, weight gain, and adiposity during an ad libitum feeding challenge accompanied by decreased insulin response to an intravenous glucose tolerance test.

Indexed as

Prenatal Exposure Delayed EffectsAdiposityAnimalsAppetiteDexamethasoneFeeding BehaviorFemaleGlucocorticoidsGlucoseGlucose IntoleranceGlucose Tolerance TestHydrocortisoneLeptinPregnancySheepWeight GainDexamethasoneGlucocorticoidsGlucoseHydrocortisoneLeptinappetitefetalleptinmultigenerationalsheepsynthetic glucocorticoids

Identifiers

PMID23727517
PMCPMC3786012
OpenAlexW1986090235

What OpenQuestion holds

Textmetadata
LicenceTDM
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.