Evidence map›Paper›PMID 22067322›Full record

ArticleEndocrinology2012

Prenatal dexamethasone exposure potentiates diet-induced hepatosteatosis and decreases plasma IGF-I in a sex-specific fashion.

David L Carbone, Damian G Zuloaga, Ryoko Hiroi, Chad D Foradori, Marie E Legare, Robert J Handa

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.6field-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

31 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Prenatal dexamethasone programs autonomic dysregulation in female rats.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  3. Article
  4. Article
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  8. Review
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  11. Review
  12. Article
  13. Sex differences in major depression and comorbidity of cardiometabolic disorders: impact of prenatal stress and immune exposures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Review
  14. Insulin-Like Growth Factor (IGF) System in Liver Diseases.International journal of molecular sciences · 2018
    Review
  15. Article
  16. Review
  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

6 authors at 2 institutions in 1 country.

David L CarboneDepartment of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, 425 North 5th Street, Phoenix, Arizona 85004, USA. carbone@email.arizona.edu
Damian G Zuloaga
Ryoko Hiroi
Chad D Foradori
Marie E Legare
Robert J Handa
University of Arizona · USColorado State University · US

Funding

Sex-Specific Programming of the HPA Axis by GlucocorticoidsP50MH082679 · NIMH · BRIGHAM AND WOMEN'S HOSPITAL · PI GOLDSTEIN, JILL M · 2007 to 2011
$5.9M
SEX DIFFERENCES IN HYPOTHALAMO-PITUITARY-ADRENAL AXISR01NS039951 · NINDS · UNIVERSITY OF ARIZONA · PI HANDA, ROBERT J · 2001 to 2013
$4.3M
NIMH NIH HHS MH082679NIMH NIH HHS P50 MH082679NINDS NIH HHS NS039951NINDS NIH HHS R01 NS039951
6 · The paper itself

Abstract

The clinical use of synthetic glucocorticoids in preterm infants to promote lung development has received considerable attention due to the potential for increased risk of developing metabolic disease in adulthood after such treatment. In this study, we examined the hypothesis that exposure to the synthetic glucocorticoid, dexamethasone (DEX), during late gestation in the rat results in the development of nonalcoholic fatty liver disease in adult offspring. Pregnant Sprague Dawley dams were treated with 0.4 mg/kg DEX beginning on gestational d 18 until parturition (gestational d 23). At postnatal d 21, offspring were weaned onto either a standard chow or high-fat (60% fat-derived calories) diet. In adulthood (postnatal d 60-65), hepatic tissue was harvested and examined for pathology. Liver steatosis, or fat accumulation, was found to be more severe in the DEX-exposed female offspring that were weaned onto the high-fat diet. This finding corresponded with decreased plasma IGF-I concentrations, as well as decreased hypothalamic expression of GHRH mRNA. Morphological measurements on body and long bone length further implicate a GH signaling deficit after fetal DEX exposure. Collectively, these data indicate suppression of GH axis function in the female DEX/high-fat cohort but not in the male offspring. Because deficits in the GH signaling can be linked to the development of nonalcoholic fatty liver disease, our results suggest that the prominent liver injury noted in female offspring exposed to DEX during late gestation may stem from abnormal development of the GH axis at the hypothalamic level.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsBase SequenceBone DevelopmentDexamethasoneDiet, High-FatFatty LiverFemaleGestational AgeGrowth HormoneHumansHypothalamusInfant, NewbornInsulin-Like Growth Factor IMaleNon-alcoholic Fatty Liver DiseaseDexamethasoneGrowth HormoneInsulin-Like Growth Factor IRNA, Messenger

Identifiers

PMID22067322
PMCPMC3249671
OpenAlexW2047996813

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.