6 citations
,
October 2018 in “Endocrinology” This study indicates that sheep prenatally androgenized with testosterone show wool fiber diameter changes that parallel the increased hair diameter in women with polycystic ovary syndrome.
430 citations
,
July 2002 in “Journal of Endocrinology” This hypothesis paper suggests that PCOS may result from genetically determined ovarian hypersecretion of androgens, influencing hormone regulation and insulin resistance, with obesity further affecting its severity; no new clinical results are reported.
253 citations
,
March 2006 in “The Journal of Clinical Endocrinology and Metabolism” This review discusses the hypothesis that polycystic ovary syndrome may originate in fetal life due to prenatal androgen exposure, but reports no new clinical results.
February 2023 in “Frontiers in Endocrinology” In this study, prenatal androgen exposure was linked to altered sexual behaviors in both male and female mice, with specific effects on mounting and lordosis behaviors.
3 citations
,
March 2024 in “Frontiers in Cell and Developmental Biology” This study observed that both prenatal androgen exposure and postnatal early-life environment influence the development of PCOS-like phenotypes and changes in the gut microbiota in prenatally androgenized offspring.
32 citations
,
February 2017 in “Human Reproduction” This study found that women with PCOS were more likely to have longer anogenital distances, indicating possible intrauterine origins linked to prenatal androgen exposure.
25 citations
,
June 2012 in “Endocrine” This review discusses emerging concepts in PCOS from the AEPCOS 2010 meeting and reports no clinical findings; it suggests that the transition of care in congenital adrenal hyperplasia could inform PCOS adolescent care.
26 citations
,
November 1993 in “Progress in Neuro-psychopharmacology & Biological Psychiatry” This study reported that prenatal exposure to dihydrotestosterone altered long-term androgen metabolism in juvenile male rats, suggesting different regulatory mechanisms for 5a-reductase in hypothalamic versus pituitary tissues.
8 citations
,
February 2010 in “Journal für Kardiologie (Krause & Pachernegg GmbH)” This study developed a detailed classification system for functional androgenization in females that may enhance diagnosis and personalized treatment by identifying individual dysfunctions.
991 citations
,
January 2011 in “Nature Reviews Endocrinology” This paper reviews the diagnostic criteria, associated morbidities, and possible evolutionary advantages of polycystic ovary syndrome, but does not report any new findings.
16 citations
,
September 2018 in “Clinical Biochemistry” This paper discusses the link between polycystic ovarian syndrome (PCOS) and health issues like infertility and cardiovascular diseases, caused by both genetic and environmental factors, but reports no new clinical findings.
232 citations
,
December 2005 in “Andrology” This review explores the hypothesis that polycystic ovary syndrome may originate in fetal life due to genetic predispositions and environmental influences, but it reports no new clinical findings.
January 2021 in “Deep Blue (University of Michigan)” This study found that LepRb neurons in the brain are important targets for androgen action and influence sex-specific differences in reproductive and metabolic regulation, implicating them in conditions such as polycystic ovary syndrome.
5 citations
,
May 2019 in “Anais Brasileiros de Dermatologia” This article discusses the connection between prenatal androgen exposure, marked by the second-to-fourth digit ratio, and seborrheic dermatitis, but reports no new experimental findings.
21 citations
,
July 2019 in “Cardiovascular Research” This study found that prenatal exposure to androgens caused long-lasting heart remodeling and left ventricular hypertrophy in female mice offspring, suggesting potential cardiac risks for daughters of mothers with PCOS.
2 citations
,
August 2023 in “Journal of Endocrinological Investigation” In this study, researchers found that pregnant mice exposed to excessive androgen led to thinner ventricular walls and cardiac hypertrophy in offspring, suggesting that prenatal androgen exposure adversely affects cardiac health through reduced cardiomyocyte proliferation.
1 citations
,
June 2023 in “Reproduction” This review discusses the role of microglia in mediating prenatal androgen effects on the female brain, potentially contributing to PCOS development and neuroendocrine dysfunctions, but reports no new results.
November 2023 in “International journal of reproduction, contraception, obstetrics and gynecology” This review discusses the hypotheses surrounding the developmental origins of polycystic ovary syndrome, particularly the role of prenatal androgen exposure, and reports no new experimental results.
29 citations
,
February 2018 in “Genetics research international” This review summarizes the influence of gene polymorphisms on genetic predisposition to polycystic ovary syndrome, but reports no new experimental or clinical results.
10 citations
,
February 2007 in “Current Opinion in Endocrinology, Diabetes and Obesity” This review discusses the early developmental origin of premature adrenarche and polycystic ovary syndrome and highlights potential utero-based mechanisms, reporting no new clinical findings.
258 citations
,
July 2016 in “Reproductive Biology and Endocrinology” This abstract reviews the characteristics and health risks associated with polycystic ovary syndrome and does not report new findings, highlighting the syndrome's multifactorial nature.
44 citations
,
May 2012 in “Endocrinology” This review discusses the etiology of polycystic ovary syndrome, emphasizing the role of genetic and environmental factors, and reports no new experimental findings.
11 citations
,
August 2019 in “The Journal of Sexual Medicine” This study found that women with nonclassic congenital adrenal hyperplasia (NC-CAH) reported lower sexual function and higher sexual distress compared to those with classic CAH (C-CAH), particularly among those showing signs of androgen excess.
51 citations
,
January 2003 in “Hormone Research in Paediatrics” This review discusses hormonal influences on hair growth and suggests that understanding hormone-gene interactions may improve treatment of hirsutism and alopecia, but reports no new clinical findings.
December 2023 in “Frontiers in endocrinology” This review explores the role of hyperandrogenism, including adrenal-derived 11-oxygenated androgen, in the development of polycystic ovarian syndrome and discusses potential therapeutic strategies targeting androgen excess, without reporting new clinical results.
November 2016 in “Elsevier eBooks” This chapter reviews genetic defects in female sexual differentiation, focusing on 46,XX disorders of sex development and the impact of genetic factors and sex steroids on development, but reports no new clinical findings.
883 citations
,
August 2016 in “Nature Reviews Disease Primers” This review discusses the current understanding of polycystic ovary syndrome, focusing on its epidemiology, pathophysiology, diagnosis, management, and future research directions, but reports no new clinical results.
343 citations
,
December 2008 in “Endocrine Reviews” This review discusses the various evidence-based and potential applications of metformin in treating and preventing symptoms and complications associated with polycystic ovary syndrome but reports no new clinical results.
124 citations
,
June 2002 in “Best Practice & Research Clinical Endocrinology & Metabolism” This article reviews polycystic ovary syndrome in adolescents, highlighting its endocrine and metabolic features, and reports no new clinical findings; the etiology may involve early-life abnormalities in androgen production.
71 citations
,
November 2009 in “Best Practice & Research in Clinical Obstetrics & Gynaecology” This article discusses the complexities of diagnosing and managing polycystic ovary syndrome in adolescents and highlights the lack of established diagnostic criteria and unclear clinical implications, without presenting new clinical findings.