ArticleThe Journal of endocrinology2010
Prenatal androgen exposure programs metabolic dysfunction in female mice.
Article in The Journal of endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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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.
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Who cites it
114 citing papers in PubMed, 181 citations in OpenAlex.
- Hypoadiponectinemia does not enhance anxiety-like behaviour in a lean PCOS-like mouse model.Scientific reports · 2026Article
- Ovarian insulin signaling is intact despite systemic insulin resistance in a mouse model of polycystic ovary syndrome.Endocrinology · 2026Article
- Excess female adrenal androgen secretion is a consequence of in utero androgenic excess in sheep.Reproduction & fertility · 2026Article
- Butyric acid-based self-assembling nanoparticles: a potential strategy to prevent development of polycystic ovary syndrome.Molecular human reproduction · 2026Article
- Developmental programming: Differing impact of prenatal testosterone and prenatal bisphenol-A -treatment on hepatic methylome in female sheep.Molecular and cellular endocrinology · 2025Article
- POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Genetics of polycystic ovary syndrome (PCOS).Reproduction (Cambridge, England) · 2025Review
- Chemically-induced histopathological progression in the polycystic ovary syndrome (PCOS)- A review.Toxicological research · 2025Review
- Prenatally androgenized PCOS mice have ovary-independent uterine dysfunction and placental inflammation aggravated by high-fat diet.Science advances · 2025Article
- The Molecular Basis of Polycystic Ovary Syndrome and Its Cardiometabolic Correlates: Exploring the Intersection and Its Clinical Implications-A Narrative Review.Biomedicines · 2025Review
- Impaired glucose tolerance and insulin resistance in a prenatally-androgenized rat model of polycystic ovary syndrome in later life.Experimental physiology · 2025Article
- Article
- Sulfation pathways in the maintenance of functional beta-cell mass and implications for diabetes.Essays in biochemistry · 2024Review
- Preconceptional maternal hyperandrogenism and metabolic syndrome risk in male offspring: a long-term population-based study.Journal of endocrinological investigation · 2024Article
- Maternal high fat diet induces circadian clock-independent endocrine alterations impacting the metabolism of the offspring.iScience · 2024Article
- Developmental programming: Testosterone excess masculinizes female pancreatic transcriptome and function in sheep.Molecular and cellular endocrinology · 2024Article
- Association between single nucleotide polymorphisms, TGF-β1 promoter methylation, and polycystic ovary syndrome.BMC pregnancy and childbirth · 2024Article
- Metabolic characteristics of different phenotypes in reproductive-aged women with polycystic ovary syndrome.Frontiers in endocrinology · 2024Article
- Age-Dependent Changes in the Effects of Androgens on Female Metabolic and Body Weight Regulation Systems in Humans and Laboratory Animals.International journal of molecular sciences · 2023Review
- The Influences of Perinatal Androgenic Exposure on Cardiovascular and Metabolic Disease of Offspring of PCOS.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Maternal androgen excess increases the risk of metabolic syndrome in female offspring in their later life: A long-term population-based follow-up study.Archives of gynecology and obstetrics · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a common fertility disorder with metabolic sequelae. Our laboratory previously characterized reproductive phenotypes in a prenatally androgenized (PNA) mouse model for PCOS. PNA mice exhibited elevated testosterone and LH levels, irregular estrous cycles, and neuroendocrine abnormalities suggesting increased central drive to the reproductive system. In this study, we examined metabolic characteristics of female PNA mice. PNA mice exhibited increased fasting glucose and impaired glucose tolerance (IGT) that were independent of age and were not associated with changes in body composition or peripheral insulin sensitivity. IGT was associated with defects in pancreatic islet function leading to an impaired response to high glucose, consistent with impaired insulin secretion. Exposure of isolated pancreatic islets to androgen in vitro demonstrated an impaired response to glucose stimulation similar to that in PNA mice, suggesting androgens may have activational in addition to organizational effects on pancreatic islet function. PNA mice also exhibited increased size of visceral adipocytes, suggesting androgen-programed differences in adipocyte differentiation and/or function. These studies demonstrate that in addition to causing reproductive axis abnormalities, in utero androgen exposure can induce long-term metabolic alterations in female mice.
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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.