<unk>  ovaries develop when the ovaries are stimulated to produce excessive amounts of androgenic hormones, in particular testosterone, by either one or a combination of the following (almost certainly combined with genetic susceptibility): * the release of excessive luteinizing hormone (LH) by the anterior pituitary gland * through high levels of insulin in the blood (hyperinsulinaemia) in women whose ovaries are sensitive to this stimulus The<unk>  acquired its most widely used name due to the common sign on ultrasound examination of multiple (poly) ovarian cysts. These "cysts" are actually immature follicles not cysts. The follicles have developed from primordial follicles, but the development has stopped ("arrested") at an early antral stage due to the disturbed ovarian function. The follicles may be oriented along the ovarian periphery, appearing as a 'string of pearls' on ultrasound examination. Women with<unk>  experience an increased frequency of hypothalamic GnRH pulses, which in turn results in an increase in the LH/FSH ratio. A majority of women with<unk>  have insulin resistance and/or are obese. Their elevated insulin levels contribute to or cause the abnormalities seen in the hypothalamic-pituitary-ovarian axis that lead to<unk> . Hyperinsulinemia increases GnRH pulse frequency; LH over FSH dominance; increased ovarian androgen production; decreased follicular maturation; and decreased SHBG binding. Furthermore, excessive insulin, acting through its cognate receptor in the presence of component cAMP signalling, upregulates 17α-hydroxylase activity via PI3K, 17α-hydroxylase activity being responsible for synthesising androgen precursors. The combined effects of hyperinsulinemia contribute to an increased risk of<unk> . Insulin resistance is a common finding among women with a normal weight as well as overweight women. Adipose tissue<unk> sesses aromatase, an enzyme that converts androstenedione to estrone and testosterone to estradiol. The excess of adipose tissue in obese women creates the paradox of having both excess androgens (which are responsible for hirsutism and virilization) and estrogens (which inhibits FSH via negative feedback).<unk>  may be associated with chronic inflammation, with several investigators correlating inflammatory mediators with anovulation and other<unk>  symptoms. Similarly, there seems to be a relation between<unk>  and increased level of oxidative stress. It has previously been suggested that the excessive androgen production in<unk>  could be caused by a decreased serum level of IGFBP-1, in turn increasing the level of free IGF-I, which stimulates ovarian androgen production, but recent data concludes this mechanism to be unlikely.<unk>  has also been associated with a specific FMR1 sub-genotype. The research suggests that women with heterozygous-normal/low FMR1 have<unk> -like symptoms of excessive follicle-activity and hyperactive ovarian function.
Polycystic ovary syndrome
Hypothyroidism
Gonadotropin-resistant ovary syndrome
Hyperprolactinaemia
Functional hypothalamic amenorrhea
Congenital adrenal hyperplasia
Lactational amenorrhea
Metabolic syndrome