ArticleThe Journal of steroid biochemistry and molecular biology2021
Fetal programming of polycystic ovary syndrome: Effects of androgen exposure on prenatal ovarian development.
Article in The Journal of steroid biochemistry and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Chronic inflammatory activity in women with normogonadotropic anovulation complicated by subclinical thyroid dysfunction: a prospective cohort study.Frontiers in endocrinology · 2026Article
- Is polycystic ovary syndrome associated with uterine malformations? A systematic review using Bradford Hill's causality framework.Human reproduction open · 2026Review
- Analysis of factors influencing polycystic ovary syndrome in women of reproductive age based on directed acyclic graphs.Scientific reports · 2025Article
- Prenatal exposure to a single dose of testosterone adversely affects the oocyte and embryo quality in rats during adulthood: An experimental study.International journal of reproductive biomedicine · 2025Article
- Ovarian function measures in normogonadotropic anovulation and subclinical thyroid dysfunction: a prospective cohort study.Endocrine · 2025Article
- Associations of maternal per- and polyfluoroalkyl substance plasma concentrations during pregnancy with offspring polycystic ovary syndrome and related characteristics in project viva.Environmental research · 2025Article
- Preconceptional maternal hyperandrogenism and metabolic syndrome risk in male offspring: a long-term population-based study.Journal of endocrinological investigation · 2024Article
- Transient clitoromegaly in an extremely preterm twin infant with popliteal pterygium.Pediatric endocrinology, diabetes, and metabolism · 2024Article
- Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology.International journal of molecular sciences · 2023Review
- Immune Dysfunction in Polycystic Ovary Syndrome.ImmunoHorizons · 2023Review
- Ovarian expression of follicle stimulating hormone and activin receptors genes in a prenatally-androgenized rat model of polycystic ovary syndrome in adulthood.Molecular biology reports · 2022Article
- Somatic cell fate maintenance in mouse fetal testes via autocrine/paracrine action of AMH and activin B.Nature communications · 2022Article
- Review
- Maternal low protein diet and fetal programming of lean type 2 diabetes.World journal of diabetes · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a common form of anovulatory infertility with a strong hereditary component but no candidate genes have been found. The inheritance pattern may be due to in utero androgen programming on gene expression and mitochondria. Mitochondria are maternally inherited and alterations to mitochondria after fetal androgen exposure may explain one of the mechanisms of fetal programming in PCOS. Our aim was to investigate the role of excessive prenatal androgens in ovarian development by identifying how hyperandrogenemia affects gene expression and mitochondria in neonatal ovary. Pregnant dams were injected with dihydrotestosterone on days 16-18 of pregnancy. Day 0 ovaries were collected for gene expression and mitochondrial studies. RNAseq showed differential gene expressions which were related to mitochondrial dysfunction, fetal gonadal development, oocyte maturation, metabolism, angiogenesis, and PCOS. Top 20 up and downregulated genes were validated with qPCR and Western Blot. Transcriptional pathways involved in folliculogenesis and genes involved in ovarian and mitochondrial function were dysregulated. Further, DHT exposure altered mitochondrial ultrastructure and function by increasing mitochondrial oxygen consumption and decreasing mitochondrial efficiency with increased proton leak within the first day of life. Our data indicates that one path that leads to PCOS begins at birth and is programmed in utero by androgens.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.