Evidence map›Paper›PMID 18948400›Full record

ArticleEndocrinology2009

Facilitative glucose transporter type 1 is differentially regulated by progesterone and estrogen in murine and human endometrial stromal cells.

Antonina Frolova, Lauren Flessner, Maggie Chi, Sung Tae Kim, Nastaran Foyouzi-Yousefi, Kelle H Moley

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

54 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Glucose metabolism and endometrium decidualization.Frontiers in endocrinology · 2025
    Review
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  6. Article
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  18. Article
  19. Endometrial Glucose Transporters in Health and Disease.Frontiers in cell and developmental biology · 2021
    Review
  20. 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

6 authors at 1 institution in 1 country.

Antonina FrolovaDepartment of Obstetrics and Gynecology, Washington University School of Medicine, St Louis, Missouri 63110, USA.
Lauren Flessner
Maggie Chi
Sung Tae Kim
Nastaran Foyouzi-Yousefi
Kelle H Moley
Washington University in St. Louis · US

Funding

GLUTS AND GLUCOSE TRANSPORT IN THE MOUSE BLASTOCYSTR01HD040390 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2012
$2.6M
IGF Induced Toxicity in Preimplantation EmbryosR01DK070351 · NIDDK · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2004 to 2007
$1.4M
Molecular Aspects of ImplantationR01HD040810 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2006
$1.2M
NICHD NIH HHS HD040390NICHD NIH HHS HD040810NICHD NIH HHS R01 HD040390NICHD NIH HHS R01 HD040810NIDDK NIH HHS DK070351NIDDK NIH HHS R01 DK070351
6 · The paper itself

Abstract

Embryo implantation is a highly synchronized event between an activated blastocyst and a receptive endometrium. The success of this process relies on the dynamic interplay of estrogen (E(2)) and progesterone (P(4)), however, the details of this interaction are not entirely clear. Recent data implicate E(2) and P(4) in the regulation of glucose utilization by affecting facilitative glucose transporter (GLUT) expression. In this study we examine GLUT1 expression in murine and human endometrial stromal cells (ESCs) using a primary culture system. We show that expression of GLUT1 is increased during ESC decidualization in vitro. P(4) up-regulates, whereas E(2) down-regulates, GLUT1 expression. In addition, P(4) increases and E(2) decreases glucose uptake in ESCs, suggesting that GLUT1 may be a major player in glucose utilization in these cells. Moreover, GLUT1 expression is increased in human ESCs when decidualized in vitro with P(4) and dibutyryl cAMP, suggesting a similar role for P(4) in human endometrium. In conclusion, an imbalance between P(4) and E(2) seen in patients with polycystic ovary syndrome, luteal phase defect, and recurrent pregnancy loss may have a critical impact on glucose utilization in the endometrial stroma, and, thus, may be responsible for endometrial dysfunction and failure of embryo implantation in these patient populations.

Indexed as

AnimalsBucladesineCells, CulturedDeciduaEmbryo ImplantationEndometriumEstradiolFemaleGene Expression RegulationGlucose Transporter Type 1HumansMiceMice, Inbred C57BLPregnancyProgesteroneStromal CellsBucladesineEstradiolGlucose Transporter Type 1Progesterone

Identifiers

PMID18948400
PMCPMC2654750
OpenAlexW2069961599

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.