Evidence map›Paper›PMID 32678007›Full record

ArticleClinical epigenetics2020

IGF1 gene is epigenetically activated in preterm infants with intrauterine growth restriction.

Masato Kantake, Naho Ikeda, Hirofumi Nakaoka, Natsuki Ohkawa, Toshitaka Tanaka, Kazuki Miyabayashi, Hiromichi Shoji, Toshiaki Shimizu

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2020. 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
2.6field-weighted citation impact, top 11% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. 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

8 authors at 3 institutions in 1 country.

Masato KantakeNeonatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan. kantake@juntendo.ac.jp.ORCID 0000-0002-9392-3562
Naho IkedaNeonatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan.
Hirofumi NakaokaHuman Genetics Laboratory, Department of Genomics and Evolutionary Biology, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka, 411-8540, Japan.
Natsuki OhkawaNeonatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan.
Toshitaka TanakaPerinatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan.
Kazuki MiyabayashiNeonatal Medical Center, Juntendo University Shizuoka Hospital, 1192 Nagaoka, Izunokuni, Shizuoka, 410-2295, Japan.
Hiromichi ShojiDepartment of Pediatrics and Adolescent Medicine, Juntendo University, 3-1-3 Hongo, Bunkyo-ku, Tokyo, 113-8431, Japan.
Toshiaki ShimizuDepartment of Pediatrics and Adolescent Medicine, Juntendo University, 3-1-3 Hongo, Bunkyo-ku, Tokyo, 113-8431, Japan.
Juntendo University Shizuoka Hospital · JPJuntendo University · JPNational Institute of Genetics · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIGF1 is a key molecule in the regulation of growth and metabolism. Low IGF1 secretion is known to cause growth restriction in childhood, as well as deregulated lipid metabolism, cardiovascular disease, and diabetes in adulthood. The IGF1 gene P2 promoter is highly methylated, resulting in low secretion of IGF1 in small infants and children. However, it is unknown when this methylation occurs. The aim of study was to clarify the point when this epigenetic program occurs during intrauterine development. We analyzed 56 preterm infants born before 32 weeks of gestation, including 19 intrauterine growth restriction (IUGR) infants whose birth weights were lower than - 2SD calculated by the Japanese datasets. We extracted genomic DNA from whole blood at birth; methylation of the six CpG sites in the IGF1 P2 promoter was analyzed by the bisulfite amplicon method using the MiSeq platform.

resultsIn contrast to term infants and children, the methylation of all six CpG sites positively correlated with body weight and body length at birth. IGF1 P2 promoter methylation levels were significantly reduced in all six CpG sites in infants with IUGR.

conclusionsThese findings indicated that the IGF1 gene is epigenetically activated before 32 weeks of gestation in infants with IUGR and that the activated gene may become suppressed after this time point. This study may provide new insights to prevent the onset of adult diseases and to aid in nutritional management for preterm birth infants in neonatal intensive care units.

Indexed as

AdultCardiovascular DiseasesCase-Control StudiesChildCpG IslandsDiabetes MellitusDNA MethylationEpigenomicsFemaleFetal Growth RetardationGestational AgeHumansInfant, NewbornInfant, PrematureInfant, Small for Gestational AgeInsulin-Like Growth Factor IIGF1 protein, humanInsulin-Like Growth Factor IEpigeneticsIGF1Intrauterine growth restrictionIUGRMethylationNewborn infantP2 promoterPreterm

Identifiers

PMID32678007
PMCPMC7364555
OpenAlexW3043393580

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.