The role of gonadotropin‐releasing hormone neurons in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder seen in the clinic, with a prevalence depending on the diagnostic criteria utilized. 1 PCOS affects approximately 10% of women according to the currently-recommended Rotterdam diagnostic criteria, which include evidence of at least two of the following: clinical and/or biochemical hyperandrogenism, chronic oligo-or anovulation, and polycystic ovarian morphology. [1][2][3] The prevalence of PCOS is approximately 6% according to the classic National Institutes of Health (NIH) definition of PCOS, which mandates both hyperandrogenism and ovulatory dysfunction. 1,4 Finally, PCOS affects approximately 10% of women according to the Androgen Excess and PCOS Society criteria: hyperandrogenism plus either ovulatory dysfunction or polycystic ovarian morphology. 1,5 PCOS has also been associated with several comorbidities, including obesity, insulin resistance and type 2 diabetes, depression and anxiety, obstructive sleep apnea, and endometrial cancer. [6][7][8][9][10][11][12] Although the characteristics that define PCOS (i.e., androgen excess, oligo-/anovulation and polycystic ovarian morphology) are most directly related to ovarian function, the central reproductive neuroendocrine system, particularly the gonadotropin-releasing

Prenatal androgen treatment impairs the suprachiasmatic nucleus arginine-vasopressin to kisspeptin neuron circuit in female mice

“…Although the reproductive symptoms of PCOS are expressed in the periphery, some of these dysfunctions may have a central origin. Indeed, ovarian dysfunction in PCOS is thought to be brought about by impaired feedback regulation of the pulsatile gonadotropin-releasing hormone (GnRH) neuron drive on anterior pituitary gonadotropin release, causing follicular arrest and elevated androgen secretion (1,5).…”

A review of the hormones involved in the endocrine dysfunctions of polycystic ovary syndrome and their interactions

“…In women with PCOS, the androgen receptor may experience increased activity in the hypothalamus, ovary, skeletal muscle or adipose cells ( 21 ). High androgens in PCOS at least partially contribute to an increase in GnRH/LH pulse frequency ( 1 , 22 ) and vice versa, generating a cycle of hormonal dysregulation ( 23 ). Functional ovarian hyperandrogenism can be directly or indirectly identified in the vast majority of PCOS patients ( 1 ).…”

“…Elevated serum LH concentration is closely associated with a reduced chance of conception and an increased risk of miscarriage ( 42 ). However, it is unclear how substantially excessive LH in PCOS contributes to ovarian dysfunction ( 23 ).…”

Enhanced pup retrieval behaviour in a mouse model of polycystic ovary syndrome

“…This condition, characterised by oligo‐ or anovulation, polycystic ovarian morphology and hyperandrogenism, 3 is associated with high rates of sub or infertility as well as metabolic complications 4 . Clearly, PCOS pathology involves several different organ systems, including the ovaries and brain 5,6 . A hallmark feature of PCOS, 7 hyperandrogenism, is also hypothesised to be an underlying mechanism driving the development of the condition in utero 8–10 .…”

“…4 Clearly, PCOS pathology involves several different organ systems, including the ovaries and brain. 5,6 A hallmark feature of PCOS, 7 hyperandrogenism, is also hypothesised to be an underlying mechanism driving the development of the condition in utero. [8][9][10] In women with PCOS, hyperandrogenaemia is found in 60%-80% of women, and hyperandrogenaemia remains significantly elevated during pregnancy.…”