Evidence map›Paper›PMID 21325042›Full record

ArticleEndocrinology2011

Maternal ghrelin deficiency compromises reproduction in female progeny through altered uterine developmental programming.

J Ryan Martin, Sarah B Lieber, James McGrath, Marya Shanabrough, Tamas L Horvath, Hugh S Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Role of the Gastric Hormones Ghrelin and Nesfatin-1 in Reproduction.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Ghrelin: ghrelin as a regulatory Peptide in growth hormone secretion.Journal of clinical and diagnostic research : JCDR · 2014
    Review
  8. Review
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 1 institution in 1 country.

J Ryan MartinDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Sarah B Lieber
James McGrath
Marya Shanabrough
Tamas L Horvath
Hugh S Taylor
Yale University · US

Funding

Tissue Factor and EmdometriosisU54HD052668 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH · 2007 to 2011
$6.6M
HOX Gene Expression by Endocrine Disrupting ChemicalsR01ES010610 · NIEHS · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH · 2001 to 2011
$2.9M
Hox Gene Expression in Human EndometriumR01HD036887 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH S · 2003 to 2007
$1.4M
HOX GENE EXPRESSION IN HUMAN ENDOMETRIUMR29HD036887 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH S · 1998 to 2002
$352k
NICHD NIH HHS HD036887NICHD NIH HHS HD052668NICHD NIH HHS R01 HD036887NICHD NIH HHS R29 HD036887NICHD NIH HHS U54 HD052668NIEHS NIH HHS ES010610NIEHS NIH HHS R01 ES010610
6 · The paper itself

Abstract

Ghrelin has a well-known role in the regulation of appetite, satiety, energy metabolism, and reproduction; however ghrelin has not been implicated in reproductive tract development. We examined the effect of ghrelin deficiency on the developmental programming of female fertility. We observed that female wild-type mice born of ghrelin heterozygote dams (i.e. exposed in utero to ghrelin deficiency) had diminished fertility and produced smaller litters. We demonstrate that exposure to in utero ghrelin deficiency led to altered developmental programming of the reproductive tract. The number of ovarian follicles, corpora lutea, and embryos produced were identical in both exposed and unexposed mice. However wild-type embryos transferred to uteri of mice exposed to in utero ghrelin deficiency had a 60% reduction in the rate of embryo implantation compared with those transferred to wild-type unexposed uteri. We identified significant alterations in the uterine expression of four genes critical for implantation and a defect in uterine endometrial proliferation. Taken together, these results demonstrate that the mechanism of subfertility was abnormal endometrial function. In utero exposure to decreased levels of ghrelin led to defects in developmental programming of the uterus and subsequent subfertility in wild-type offspring.

Indexed as

AnimalsEmbryo ImplantationEmpty Spiracles Homeobox ProteinsFemaleFertilityGene Expression Regulation, DevelopmentalGhrelinHeterozygoteHomeobox A10 ProteinsHomeodomain ProteinsImmunohistochemistryLitter SizeMaleMiceMice, KnockoutProliferating Cell Nuclear AntigenEmpty Spiracles Homeobox ProteinsGhrelinHomeobox A10 ProteinsHomeodomain ProteinsHoxa10 protein, mouseProliferating Cell Nuclear AntigenTranscription FactorsWnt7a protein, mouseWnt Proteins

Identifiers

PMID21325042
PMCPMC3075930
OpenAlexW2044475243

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.