ReviewBiochemical Society transactions2020
Androgens and the masculinization programming window: human-rodent differences.
Review in Biochemical Society transactions, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled 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.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- A Systematic Review of Anogenital Distance and Gynecological Disorders: Endometriosis and Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Pooled it
- Revisiting the dual role of androgens and oestrogens in mammalian sex differentiation with a focus on genitalia.Nature reviews. Urology · 2026Review
- Hypothalamic neurovascular and extracellular matrix remodeling: Cellular niche orchestration of immune-metabolic adaptation to nutritional stress.Reviews in endocrine & metabolic disorders · 2026Review
- Androgen signaling is dispensable for fetal testis formation: decoupling testis organogenesis from fetal masculinization programming.Molecular human reproduction · 2026Review
- Sexual dimorphism in the development and function of the melanocortin system.Reviews in endocrine & metabolic disorders · 2026Review
- Anogenital distance in patients with Klinefelter syndrome.Clinical and experimental reproductive medicine · 2026Article
- The ontogeny of sex differences in exercise performance.Journal of the Endocrine Society · 2026Article
- Article
- Review
- Porcine Leydig cells: central regulators of boar reproductive development and fertility.Journal of animal science · 2026Review
- Season of birth and variations in male reproductive health: A population-based cohort study.Andrology · 2026Article
- Fetal exposure to a mixture of endocrine-disrupting chemicals and biomarkers of male fecundity: A population-based cohort study.Andrology · 2026Article
- Perinatal exposure to the environmental pollutant butyl benzyl phthalate (BBP) induces sex-specific alterations in the neuro-immune-endocrine network in adult rats.Frontiers in immunology · 2026Article
- Testicular organoid models in male reproductive toxicology: advances, applications, and future perspectives.Frontiers in physiology · 2026Article
- Genetic, Epigenetic, and Non-Genetic Factors in Testicular Dysgenesis Syndrome: A Narrative Review.Genes · 2025Review
- Crucial roles of mesenchymalProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Prenatal Low Testosterone Levels Induced byBiomedicines · 2025Article
- Genetic variants (LhcgrBiology of sex differences · 2025Article
- The Role of Environmental Endocrine Disruptors on Leydig Cell Death and Senescen.The world journal of men's health · 2025Review
- Neuroactive steroid exposure impacts neurodevelopment: Comparison of human and rodent placental contribution.Journal of neuroendocrinology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Human male reproductive disorders are common and may have a fetal origin - the testicular dysgenesis syndrome (TDS) hypothesis. In rats, experimentally induced TDS disorders result from disruption of fetal androgen production/action specifically in the masculinization programming window (MPW). MPW androgen action also programs longer anogenital distance (AGD) in male versus female rats; shorter male AGD is correlated with risk and severity of induced TDS disorders. AGD thus provides a lifelong, calibrated readout of MPW androgen exposure and predicts likelihood of reproductive dysfunction. Pregnant rat exposure to environmental chemicals, notably certain phthalates (e.g. diethyl hexl phthalate, DEHP; dibutyl phthalate, DBP), pesticides or paracetamol, can reduce fetal testis testosterone and AGD and induce TDS disorders, provided exposure includes the MPW. In humans, AGD is longer in males than females and the presumptive MPW is 8-14 weeks' gestation. Some, but not all, epidemiological studies of maternal DEHP (or pesticides) exposure reported shorter AGD in sons, but this occurred at DEHP exposure levels several thousand-fold lower than are effective in rats. In fetal human testis culture/xenografts, DEHP/DBP do not reduce testosterone production, whereas therapeutic paracetamol exposure does. In humans, androgen production in the MPW is controlled differently (human chorionic gonadotrophin-driven) than in rats (paracrine controlled), and other organs (placenta, liver, adrenals) contribute to MPW androgens, essential for normal masculinization, via the 'backdoor pathway'. Consequently, early placental dysfunction, which is affected by maternal lifestyle and diet, and maternal painkiller use, may be more important than environmental chemical exposures in the origin of TDS in humans.
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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 OpenQuestion graph.