Evidence map›Paper›PMID 25832114›Full record

ReviewNeuroendocrinology2015

Steroidogenic versus Metabolic Programming of Reproductive Neuroendocrine, Ovarian and Metabolic Dysfunctions.

Rodolfo C Cardoso, Muraly Puttabyatappa, Vasantha Padmanabhan

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuroendocrinology, 2015. 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
11.0field-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, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Impacts of Anabolic-androgenic steroid supplementation on female health and offspring: Mechanisms, side effects, and medical perspectives.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. CAnimal reproduction · 2023
    Article
  10. Review
  11. Sexual dimorphism in testosterone programming of cardiomyocyte development in sheep.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  12. Androgen-induced insulin resistance is ameliorated by deletion of hepatic androgen receptor in females.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Article
  14. Article
  15. Article
  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

3 authors at 2 institutions in 2 countries.

Rodolfo C CardosoDepartment of Pediatrics, University of Michigan, Ann Arbor, Mich., USA.
Muraly Puttabyatappa
Vasantha Padmanabhan
University of Michigan–Ann Arbor · USBeijing Obstetrics and Gynecology Hospital · CN

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
STEROIDAL AND METABOLIC MEDIATION OF NEUROENDOCRINE CIRCUITRYP01HD044232 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PADMANABHAN, VASANTHA · 2004 to 2015
$12.9M
Bisphenol-A and Reproductive DysfunctionR01ES016541 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PADMANABHAN, VASANTHA · 2009 to 2013
$2.0M
NICHD NIH HHS P01 HD044232NIDDK NIH HHS P30 DK020572NIEHS NIH HHS R01 ES016541
6 · The paper itself

Abstract

The susceptibility of the reproductive system to early exposure to steroid hormones has become a major concern in our modern societies. Human fetuses are at risk of abnormal programming via exposure to endocrine disrupting chemicals, inadvertent use of contraceptive pills during pregnancy, as well as from excess exposure to steroids due to disease states. Animal models provide an unparalleled resource to understand the developmental origin of diseases. In female sheep, prenatal exposure to testosterone excess results in an array of adult reproductive disorders that recapitulate those seen in women with polycystic ovary syndrome (PCOS), including disrupted neuroendocrine feedback mechanisms, increased pituitary sensitivity to gonadotropin-releasing hormone, luteinizing hormone excess, functional hyperandrogenism, and multifollicular ovarian morphology culminating in early reproductive failure. Prenatal testosterone treatment also leads to fetal growth retardation, insulin resistance, and hypertension. Mounting evidence suggests that developmental exposure to an improper steroidal/metabolic environment may mediate the programming of adult disorders in prenatal testosterone-treated females, and these defects are maintained or amplified by the postnatal sex steroid and metabolic milieu. This review addresses the steroidal and metabolic contributions to the development and maintenance of the PCOS phenotype in the prenatal testosterone-treated sheep model, including the effects of prenatal and postnatal treatment with an androgen antagonist or insulin sensitizer as potential strategies to prevent/ameliorate these dysfunctions. Insights obtained from these intervention strategies on the mechanisms underlying these defects are likely to have translational relevance to human PCOS.

Indexed as

ReproductionAnimalsDisease Models, AnimalEndocrine DisruptorsFemaleFetal DevelopmentGonadotropin-Releasing HormoneHumansMaleNeurosecretory SystemsOvaryPolycystic Ovary SyndromePregnancyPrenatal Exposure Delayed EffectsSheepSteroidsEndocrine DisruptorsGonadotropin-Releasing HormoneSteroidsTestosterone

Identifiers

PMID25832114
PMCPMC4591099
OpenAlexW2047608730

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.