Evidence map›Paper›PMID 38169733›Full record

ArticleJournal of the Endocrine Society2023

Glucocorticoid Receptor Antagonism Improves Glucose Metabolism in a Mouse Model of Polycystic Ovary Syndrome.

Sheng Li, Zhixiong Ying, Max Gentenaar, Patrick C N Rensen, Sander Kooijman, Jenny A Visser, Onno C Meijer, Jan Kroon

Abstract read
In one paragraph

Article in Journal of the Endocrine Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Sheng LiDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.
Zhixiong YingDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.ORCID https://orcid.org/0000-0002-3540-7877
Max GentenaarDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.
Patrick C N RensenDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.ORCID https://orcid.org/0000-0002-8455-4988
Sander KooijmanDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.ORCID https://orcid.org/0000-0002-0014-5571
Jenny A VisserDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, 3015 GD Rotterdam, the Netherlands.
Onno C MeijerDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.ORCID https://orcid.org/0000-0002-8394-6859
Jan KroonDepartment of Medicine, Division of Endocrinology, Leiden University Medical Center, 2333ZA Leiden, the Netherlands.ORCID https://orcid.org/0000-0001-5656-3898

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Context: Polycystic ovary syndrome (PCOS) is a complex metabolic disorder associated with obesity, insulin resistance, and dyslipidemia. Hyperandrogenism is a major characteristic of PCOS. Increased androgen exposure is believed to deregulate metabolic processes in various tissues as part of the PCOS pathogenesis, predominantly through the androgen receptor (AR). Notably, various metabolic features in PCOS are similar to those observed after excess glucocorticoid exposure. Objective: We hypothesized that glucocorticoid receptor (GR) signaling is involved in the metabolic symptoms of PCOS. Methods: In a PCOS model of chronic dihydrotestosterone (DHT) exposure in female mice, we investigated whether GR signaling machinery was (de)regulated, and if treatment with a selective GR antagonist alleviated the metabolic symptoms. Results: We observed an upregulation of GR messenger RNA expression in the liver after DHT exposure. In white adipose tissues and liver we found that DHT upregulated Conclusion: We conclude that GR activation may play a role in glucose metabolism in DHT-exposed mice.

Indexed as

androgen receptordihydrotestosteroneglucocorticoid receptormetabolismpolycystic ovary syndrome

Identifiers

PMID38169733
PMCPMC10758754

What Socratic 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 Socratic graph.