Formation and early development of follicles in the polycystic ovary

Webber, Lisa; Stubbs, S; Stark, Jaroslav; Trew, G.; Margara, R.; Hardy, Kate; Franks, Stephen

doi:10.1016/s0140-6736(03)14410-8

Cited by 443 publications

(284 citation statements)

References 22 publications

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“…Given that there is an increase, compared with controls, in the density of preantral follicles in tissue from women with polycystic ovaries (Webber et al 2003, these findings support the concept that aberrant follicle development in PCOS is programmed by exposure of the ovary to excess androgen during foetal life.…”

Section: Discussionsupporting

confidence: 66%

“…This takes account of possible within-sheep correlation in follicle development. We have previously published the rationale for using this approach for analysis of human ovarian samples (Webber et al 2003. Also using Stata 10, mean proportions of follicles at each stage of development, which were positive for AR or 3bHSD (with one or more positive granulosa cells (GCs)) in control and androgenised, sheep were therefore computed and compared using logistic regression (clustered by sheep).…”

Section: Discussionmentioning

confidence: 99%

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Disorders of follicle development and steroidogenesis in ovaries of androgenised foetal sheep

Comim¹,

Hardy²,

Robinson³

2015

Journal of Endocrinology

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The prenatally androgenised (PA) sheep is a well-recognised model for the study of developmental programming of adult polycystic ovary syndrome (PCOS). Most of the studies to date have involved examination of the reproductive and metabolic effects in the offspring after puberty, but more recently, it has been reported that there is disruption of follicle formation and steroid gene expression in ovaries of foetal sheep after exposure of the mother to excess androgen. Our study examines evidence for precocious primordial follicle formation at day 90 of gestation in ovaries of foetal Poll Dorset sheep. Using a specific marker of germ cells (VASA homologue protein) in ovarian sections, we found that androgenised sheep had nearly double the proportion of germ cells enclosed in follicles compared with control animals. When analysed by follicle stage, there was no significant difference between groups in the proportion of primordial follicles and growing (transitional and primary) follicles. Differences between PA and control foetal sheep were found in both mRNA and in protein expression of steroidogenic enzymes and androgen receptor. Our results in Dorset ewes are complementary to previous reports, but suggest that the timing of follicle formation and steroidogenic activity may vary between different breeds as well as in response to androgen. These data show that granulosa cells constitute a specific target for programming by androgen in utero and raise key questions about the role of exposure to androgen in utero in developmental origins of PCOS.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Disorders of follicle development and steroidogenesis in ovaries of androgenised foetal sheep

Comim¹,

Hardy²,

Robinson³

2015

Journal of Endocrinology

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“…This suggests that the ovarian aging process in PCOS women may have been slowed down, possibly due to suppressed primordial follicle outgrowth by the high levels of AMH observed in these women. However, it has also been suggested that exhaustion of the primordial follicle pool occurs later in PCOS women because their intrinsic primordial follicle pool may be increased (Webber et al 2003). Data regarding the menopausal age in PCOS women are scarce.…”

Section: Amh As a Marker For Ovarian Pathophysiologymentioning

confidence: 99%

Anti-Müllerian hormone: a new marker for ovarian function

Visser

Jong²,

Laven³

et al. 2006

Reproduction

721

455

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Anti-Mü llerian hormone (AMH) is a member of the transforming growth factor b family of growth and differentiation factors. In the ovary, AMH has an inhibitory effect on primordial follicle recruitment as well as on the responsiveness of growing follicles to follicle-stimulating hormone (FSH). The ovary-specific expression pattern in granulosa cells of growing nonselected follicles makes AMH an ideal marker for the size of the ovarian follicle pool. This review summarizes recent findings concerning AMH and its role as a marker for the quantitative aspect of ovarian reserve as well as ovarian dysfunction.

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“…It is not too difficult to identify biochemical pathways that may be disrupted in PCOS. There is evidence for an intrinsic disorder of ovarian folliculogenesis, [45][46][47] constitutive hypersecretion of androgens by theca cells 48,49 and disordered secretion and action of insulin 50 (Figure 1). There are, however, obvious problems in searching for candidate genes in PCOS: the heterogeneous nature of the syndrome has given rise disagreement about definition and diagnostic criteria; in addition expression of features of PCOS occurs predominantly in women of reproductive age and there is no clear male phenotypeFboth of which make family-based studies difficult.…”

Section: Introductionmentioning

confidence: 99%

Polycystic ovary syndrome in adolescents

2008

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Background: Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder in women and typically presents during adolescence. The clinical and biochemical presentation is heterogeneous, but elevated serum concentrations of androgens are the most consistent biochemical abnormality and may be considered to be the hallmark of the syndrome. Many women with PCOS also have insulin resistance and hyperinsulinaemia, which may contribute to the clinical and endocrine abnormalities. The aetiology of PCOS is not clear but studies in the Rhesus monkey suggest that exposure to excess androgen during intrauterine life results in many of the features of human PCOS, including ovarian dysfunction, abnormal LH secretion and insulin resistance. Objective: To review the studies from the literature, including those of the author, regarding aetiology, presentation and management of PCOS in adolescents. Results and conclusions: We have proposed that PCOS in adolescents arises as a result of a genetically determined disorder of ovarian function that results in hyper-secretion of androgens, possibly during fetal life and also during physiological activation of the hypothalamic-pituitary-ovarian in infancy and at the onset of puberty. There is plentiful evidence for a genetic basis for PCOS (it appears to be a complex endocrine disorder resulting from the effects of a several genes), but environmental factors, notably nutrition, influence the clinical and biochemical phenotype. Obesity unmasks or amplifies symptoms, endocrine and metabolic abnormalities. The increasing incidence of childhood obesity has resulted in an alarming Increase not only in distressing symptoms but also impaired glucose tolerance and even diabetes among adolescent girls with PCOS. The search for PCOS genes in this condition, that is not only heterogeneous but also presents only in women of reproductive age, is not straightforward and has produced few convincing candidates so far. In due course, however, identification of the major susceptibility loci is likely to provide key insight into the aetiology of the syndrome and improve diagnosis and management.

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Formation and early development of follicles in the polycystic ovary

Cited by 443 publications

References 22 publications

Disorders of follicle development and steroidogenesis in ovaries of androgenised foetal sheep

Disorders of follicle development and steroidogenesis in ovaries of androgenised foetal sheep

Anti-Müllerian hormone: a new marker for ovarian function

Polycystic ovary syndrome in adolescents

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