Serum Anti-Müllerian hormone (AMH) in mothers with polycystic ovary syndrome (PCOS) and their term fetuses

Detti, Laura; Christiansen, Mary E.; Francillon, Ludwig; Ikuwezunma, Gini; Diamond, Michael P.; Mari, Giancarlo; Tobiasz, Ana

doi:10.1080/19396368.2018.1537385

Cited by 30 publications

(53 citation statements)

References 38 publications

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“…PCOS signs, however, are found before puberty. Infants born to mothers with PCOS, and thus likely to exhibit PCOS themselves [17,18], demonstrate elongated anogenital distance [29] and facial sebum [30], both indicative of gestational exposure to T; they also have elevated circulating levels of ovarian antimullerian hormone (AMH) [31,32], indicative of exaggerated antral follicle numbers typical of polycystic ovaries. Peripubertal daughters of PCOS women similarly exhibit elevated AMH levels [18,33], in addition to increased circulating LH levels [18], potentially from accelerated hypothalamic gonadotropin-releasing hormone (GnRH) pulsatile release (a trait programmed in rhesus macaques by gestational T exposure or prepubertal androgen excess [34,35]), and increased proclivity for synthesizing the highly biopotent androgen, dihydrotestosterone (DHT) [36], suggesting enhanced androgen action within target tissues.…”

Section: Pcos and Its Potential Originsmentioning

confidence: 99%

“…Infant daughters of women with PCOS exhibit elongated anogenital distance [29], as do adult women with PCOS [59][60][61]. Prepubertal daughters of women with PCOS exhibit increased whole body 5alpha-reductase activity [36], enhancing target organ exposure to androgen action before menarche, while pre-and peripubertal daughters exhibit hyperandrogenism [18,33,124], including elevated 'free' T (not bound to sex hormone binding globulin, SHBG) [33], along with consistently elevated ovarian AMH levels from infancy [18,31,32] and LH hypergonadotropism during adolescence [18]. Peripubertal hyperandrogenism can persist into adulthood, associated with reduced fecundity [125], and persistent adolescent menstrual irregularities progress to a PCOS diagnosis in~57% of cases [126].…”

Section: Infant and Peripubertal Reproduction-related Endocrine And Omentioning

confidence: 99%

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Naturally Occurring and Experimentally Induced Rhesus Macaque Models for Polycystic Ovary Syndrome: Translational Gateways to Clinical Application

et al. 2019

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Indian rhesus macaque nonhuman primate models for polycystic ovary syndrome (PCOS) implicate both female hyperandrogenism and developmental molecular origins as core components of PCOS etiopathogenesis. Establishing and exploiting macaque models for translational impact into the clinic, however, has required multi-year, integrated basic-clinical science collaborations. Paradigm shifting insight has accrued from such concerted investment, leading to novel mechanistic understanding of PCOS, including hyperandrogenic fetal and peripubertal origins, epigenetic programming, altered neural function, defective oocytes and embryos, adipogenic constraint enhancing progression to insulin resistance, pancreatic decompensation and type 2 diabetes, together with placental compromise, all contributing to transgenerational transmission of traits likely to manifest in adult PCOS phenotypes. Our recent demonstration of PCOS-related traits in naturally hyperandrogenic (High T) female macaques additionally creates opportunities to employ whole genome sequencing to enable exploration of gene variants within human PCOS candidate genes contributing to PCOS-related traits in macaque models. This review will therefore consider Indian macaque model contributions to various aspects of PCOS-related pathophysiology, as well as the benefits of using macaque models with compellingly close homologies to the human genome, phenotype, development and aging.

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Section: Pcos and Its Potential Originsmentioning

confidence: 99%

Section: Infant and Peripubertal Reproduction-related Endocrine And Omentioning

confidence: 99%

Naturally Occurring and Experimentally Induced Rhesus Macaque Models for Polycystic Ovary Syndrome: Translational Gateways to Clinical Application

et al. 2019

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“…It is reported that pregnant women with PCOS have increased serum androgen levels, including androstenedione and testosterone [ 11 – 14 ], which provides a potential source of fetal androgen excess. Insulin resistance in pregnant women with PCOS can lead to hyperinsulinemia, which may contribute to fetal hyperandrogenism exposure by inhibiting placental aromatase activity [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

“…Umbilical cord blood endocrine characteristics reflect maternal, placental, and fetal endocrine conditions. Due to this, they have been used to determine the intrauterine fetal environment in recent studies on PCOS [ 11 – 13 , 15 – 18 ]. It is almost certain that dehydroepiandrosterone (DHEA) in the fetal cord blood is not related to PCOS.…”

Section: Introductionmentioning

confidence: 99%

“…However, the outcomes regarding testosterone (T) and androstenedione (ADION) are conflicting. Some studies have shown elevated T and/or ADION levels in the cord blood in the offspring of mothers with PCOS [ 15 , 16 , 18 ], but others have observed decreased ADION levels [ 13 , 17 ] or no differences [ 11 , 12 ] compared with controls.…”

Section: Introductionmentioning

confidence: 99%

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Androgen levels in the fetal cord blood of children born to women with polycystic ovary syndrome: a meta-analysis

Duan

Pei

et al. 2020

Reprod Biol Endocrinol

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Introduction Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in reproductive-aged women. It is reported that intrauterine exposure to hyperandrogenism may induce the development of PCOS and associated complications in later life. To analyze the intrauterine androgen levels in infants born to PCOS mothers, we evaluated the androgen levels in fetal cord blood through a meta-analysis of observational studies. Material and methods The following online databases were systematically searched: PubMed, EMBASE, Cochrane library databases and Web of Science up to December 2019. Human studies compared cord blood androgen levels, including testosterone (T) and androstenedione (ADION), in fetal cord blood of mothers with and without PCOS. Statistical analysis was performed in Review Manager, Version 5.3, with the inverse variance method based on a random-effects model. Results A total of 7 articles were scrutinized and a total of 570 samples including 268 female and 222 male infants were qualified for review. In the mass spectrograph (MS) subgroup, PCOS mothers showed no signs of increased T concentration in umbilical cord blood at birth (4 studies; hazard ratio [HR] = − 0.05; 95% confidence interval [CI] = [− 0.33,0.24]; I 2 = 7%; P = 0.75; fixed-effects model). ADION level tends to be lower in daughters’ cord blood of PCOS mothers (3 studies; HR = -0.59; 95%CI = [− 1.00, − 0.19]; I 2 = 0%; P = 0.004; fixed-effects model). Conclusions Fetal cord blood T level is not related to PCOS, while ADION levels tend to be lower in the cord blood of daughters born to mothers with PCOS.

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Polycystic Ovary Syndrome and the Neuroendocrine Consequences of Androgen Excess

Silva

Campbell

2022

Comprehensive Physiology

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Polycystic ovary syndrome (PCOS) is a major endocrine disorder strongly associated with androgen excess and frequently leading to female infertility. Although classically considered an ovarian disease, altered neuroendocrine control of gonadotropin-releasing hormone (GnRH) neurons in the brain and abnormal gonadotropin secretion may underpin PCOS presentation. Defective regulation of GnRH pulse generation in PCOS promotes high luteinizing hormone (LH) pulsatile secretion, which in turn overstimulates ovarian androgen production. Early and emerging evidence from preclinical models suggests that maternal androgen excess programs abnormalities in developing neuroendocrine circuits that are associated with PCOS pathology, and that these abnormalities are sustained by postpubertal elevation of endogenous androgen levels. This article will discuss experimental evidence, from the clinic and in preclinical animal models, that has significantly contributed to our understanding of how androgen excess influences the assembly and maintenance of neuroendocrine impairments in the female brain. Abnormal central gamma-aminobutyric acid (GABA) signaling has been identified in both patients and preclinical models as a possible link between androgen excess and elevated GnRH/LH secretion. Enhanced GABAergic innervation and drive to GnRH neurons is suspected to contribute to the pathogenesis and early manifestation of neuroendocrine derangement in PCOS. Accordingly, this article also provides an overview of GABA regulation of GnRH neuron function from prenatal development to adulthood to discuss possible avenues for future discovery research and therapeutic interventions.

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Serum Anti-Müllerian hormone (AMH) in mothers with polycystic ovary syndrome (PCOS) and their term fetuses

Cited by 30 publications

References 38 publications

Naturally Occurring and Experimentally Induced Rhesus Macaque Models for Polycystic Ovary Syndrome: Translational Gateways to Clinical Application

Naturally Occurring and Experimentally Induced Rhesus Macaque Models for Polycystic Ovary Syndrome: Translational Gateways to Clinical Application

Androgen levels in the fetal cord blood of children born to women with polycystic ovary syndrome: a meta-analysis

Polycystic Ovary Syndrome and the Neuroendocrine Consequences of Androgen Excess

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