Evidence map›Paper›PMID 34575930›Full record

ArticleInternational journal of molecular sciences2021

Prenatal and Postnatal Methyl-Modulator Intervention Corrects the Stress-Induced Glucocorticoid Response in Low-Birthweight Rats.

Takahiro Nemoto, Yoshihiko Kakinuma

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular Mechanisms Underlying Stress Response and Resilience.International journal of molecular sciences · 2022
    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

2 authors at 1 institution in 1 country.

Takahiro NemotoDepartment of Bioregulatory Science (Physiology), Nippon Medical School, Tokyo 113-8602, Japan.ORCID 0000-0002-0100-8763
Yoshihiko KakinumaDepartment of Bioregulatory Science (Physiology), Nippon Medical School, Tokyo 113-8602, Japan.ORCID 0000-0001-5470-9128
Nippon Medical School · JP

Funding

Japan Society for the Promotion of Science 17K10195
6 · The paper itself

Abstract

Low body weight at birth has been shown to be a risk factor for future metabolic disorders, as well as stress response abnormalities and depression. We showed that low-birthweight rats had prolonged high blood corticosterone levels after stress exposure, and that an increase in Gas5 lncRNA, a decoy receptor for glucocorticoid receptors (GRs), reduces glucocorticoid responsiveness. Thus, we concluded that dampened pituitary glucocorticoid responsiveness disturbed the glucocorticoid feedback loop in low-birthweight rats. However, it remains unclear whether such glucocorticoid responsiveness is suppressed solely in the pituitary or systemically. The expression of Gas5 lncRNA increased only in the pituitary, and the intact induction of expression of the GR co-chaperone factor Fkbp5 against dexamethasone was seen in the liver, muscle, and adipose tissue. Intervention with a methyl-modulator diet (folate, VB

Indexed as

BiomarkersBirth WeightStress, PhysiologicalStress, PsychologicalAnimalsDietary SupplementsFemaleGene ExpressionGlucocorticoidsMethylationOrgan SpecificityPituitary GlandPregnancyRatsReceptors, GlucocorticoidRNA, Small NucleolarBiomarkersGlucocorticoidsgrowth arrest specific transcript 5Receptors, GlucocorticoidRNA, Small Nucleolarglucocorticoidlong noncoding RNAnutritionpituitarystress response

Identifiers

PMID34575930
PMCPMC8466429
OpenAlexW3198380059

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.