Evidence map›Paper›PMID 31472696›Full record

ArticleJournal of ovarian research2019

Pioglitazone suppresses excessive follicular development in murine preantral follicles.

Sachiko Nagao, Tsuyoshi Baba, Yuya Fujibe, Sayaka Adachi, Keiko Ikeda, Miyuki Morishita, Yoshika Kuno, Hiroyuki Honnma, Toshiaki Endo, Tamotsu Kiya and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ovarian research, 2019. 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
0.5field-weighted citation impact, top 28% 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, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

11 authors at 2 institutions in 1 country.

Sachiko NagaoPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan. nagaos@sapmed.ac.jp.
Tsuyoshi BabaPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Yuya FujibePresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Sayaka AdachiPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Keiko IkedaPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Miyuki MorishitaPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Yoshika KunoPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Hiroyuki HonnmaSapporo ART Clinic, 1-4 North 7 West 4, Sapporo, Hokkaido, 060-0807, Japan.
Toshiaki EndoPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Tamotsu KiyaEna Ladies Clinic, Hanakawa South 9-1-86-2, Ishikari, Hokkaido, 061-3209, Japan.
Tsuyoshi SaitoPresent address: Department of Obstetrics and Gynecology, Sapporo Medical University, South 1 West 16, Sapporo, Hokkaido, 060-8543, Japan.
Sapporo Medical University · JPSapporo Science Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic ovary syndrome (PCOS) is an endocrine disease that is common in women in their reproductive period. Patients with this disease suffer from anovulation and hyperandrogenism. Ovulation induction with exogenous gonadotropin often causes ovarian hyperstimulation syndrome because many small antral follicles pause in their growth. Treatment with insulin sensitizers is reportedly effective for both anovulation associated with PCOS, and suppression of excessive follicular growth; however, the underlying mechanism of action remains unknown. Although pioglitazone is known as an insulin sensitizer, it also has a potent modulator of cell growth and apoptosis irrespective of insulin resistance. To clarify the effect of pioglitazone on follicular growth, we performed in vitro culture of murine preantral follicles. Secondary follicles (100-160 μm in diameter) isolated from 6-week-old ICR mice were individually cultured for 13 days. Culture conditions were as follows: 1) follicle-stimulating hormone (FSH; 33 mIU/mL; control), 2) FSH plus dihydrotestosterone (DHT; 500 ng/mL), 3) FSH plus pioglitazone (5 ng/mL), and 4) FSH plus DHT/pioglitazone. Survival rate and follicle diameter were evaluated, and concentrations of estradiol (E2) and vascular endothelial growth factor (VEGF) in culture media were measured. mRNA expression of various growth-promoting factors and Vegf within follicles were also assessed. Although no significant differences were observed with regard to survival rate, follicle diameters on day 13 were significantly different.Compared with the control group, the DHT group showed enhanced growth, while groups administered pioglitazone showed stagnation of the accelerated growth induced by DHT. Although DHT treatment enhanced the expression of bone morphogenetic protein 2 (Bmp2) mRNA, pioglitazone exposure suppressed induction of Bmp2 mRNA by DHT. Vegf mRNA and protein expression were also significantly reduced when pioglitazone was added to culture media containing DHT.Administration of pioglitazone negatively affected follicular growth and VEGF levels, which may suppress excessive follicular growth and prevent ovarian hyperstimulation syndrome.

Indexed as

AndrogensAnimalsBone Morphogenetic Protein 2DihydrotestosteroneEstradiolFemaleHypoglycemic AgentsMice, Inbred ICROvarian FolliclePioglitazoneVascular Endothelial Growth Factor AAndrogensBmp2 protein, mouseBone Morphogenetic Protein 2DihydrotestosteroneEstradiolHypoglycemic AgentsPioglitazoneVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseAndrogenFollicle-stimulating hormoneFollicular developmentGrowth factorsPioglitazone

Identifiers

PMID31472696
PMCPMC6717350
OpenAlexW2971045468

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.