Evidence map›Paper›PMID 32430710›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2020

Hyperandrogenic Milieu Dysregulates the Expression of Insulin Signaling Factors and Glucose Transporters in the Endometrium of Patients With Polycystic Ovary Syndrome.

Mee-Hwa Lee, Jung-Ah Yoon, Hye-Ryun Kim, Yeon Sun Kim, Sang Woo Lyu, Byung Seok Lee, Haengseok Song, Dong Hee Choi

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. The Disorders of Endometrial Receptivity in PCOS and Its Mechanisms.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. 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

8 authors.

Mee-Hwa LeeDepartment of Obstetrics and Gynecology, CHA Bundang Medical Center, CHA University, Seongnam, Korea.
Jung-Ah YoonFertility Center of CHA Gangnam Medical Center, CHA University, Seoul, Korea.
Hye-Ryun KimDepartment of Biomedical Science, CHA University, Seongnam, Korea.
Yeon Sun KimDepartment of Biomedical Science, CHA University, Seongnam, Korea.
Sang Woo LyuFertility Center of CHA Gangnam Medical Center, CHA University, Seoul, Korea.
Byung Seok LeeDepartment of Medicine, The Graduate School of Yonsei University, Seoul, Korea.
Haengseok SongDepartment of Biomedical Science, CHA University, Seongnam, Korea. hssong@cha.ac.kr.
Dong Hee ChoiFertility Center of CHA Bundang Medical Center, CHA University, Seongnam, Korea. dhchoimc@cha.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSubfertility associated with polycystic ovary syndrome (PCOS) mainly originates from oligoovulation/anovulation. Although insulin resistance and androgen excess are known to cause PCOS-associated implantation failure, the consequences of PCOS on endometrial homeostasis and pathophysiology have not been comprehensively understood. In this study, we examined whether the pathophysiologic milieu of PCOS intrinsically affects expression profiles of genes related to insulin signaling and facilitative glucose transporters (GLUTs) in the human endometrium and/or during in vitro decidualization. STUDY

designSeven healthy women with regular menstrual cycles and 13 patients with PCOS were recruited for this study. To mimic the hyperandrogenic or hyperinsulinemic milieu in the endometrium of patient with PCOS (PCOSE) in vitro, human endometrial stromal cells (hESCs) were treated with dihydrotestosterone (DHT) or insulin, respectively.

resultsIn PCOSE, messenger RNA (mRNA) levels of insulin receptor (IR), IR substrate (IRS) 1, and IRS2 were significantly increased. Furthermore, GLUT1 and GLUT12 were aberrantly increased. Chronic exposure to insulin or DHT aberrantly increased IRS1/IRS2 phosphorylation and protein levels of GLUT1 and GLUT12 in hESCs, suggesting that not only hyperinsulinemic but also hyperandrogenic conditions affect insulin signaling and glucose metabolism. The mRNA microarrays demonstrated that DHT dysregulates various gene sets, including cell cycle and glucose metabolism, in hESCs. Furthermore, DHT suppressed the expression of GLUT1 and GLUT12 as well as decidualization markers, IGFBP1 and prolactin, during in vitro decidualization.

conclusionsThe hyperandrogenic milieu affects gene expression profiles, including gene sets associated with insulin signaling, cell cycle, glucose metabolism, and/or glucose transport, in human endometrium and during in vitro decidualization.

Indexed as

AndrogensAntigens, CDCells, CulturedDihydrotestosteroneEndometriumFemaleGlucose Transport Proteins, FacilitativeHumansInsulinPolycystic Ovary SyndromeReceptor, InsulinSignal TransductionAndrogensAntigens, CDDihydrotestosteroneGlucose Transport Proteins, FacilitativeINSR protein, humanInsulinReceptor, Insulinandrogendecidualizationendometriumglucose transporterpolycystic ovary syndrome

Identifiers

PMID32430710

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.