Abstract
Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder, affecting at least 10% of women of reproductive age. PCOS is typically characterized by the presence of at least two of the three cardinal features of hyperandrogenemia (high circulating androgen levels), oligo- or anovulation, and cystic ovaries. Hyperandrogenemia increases the severity of the condition and is driven by increased luteinizing hormone (LH) pulse secretion from the pituitary. Indeed, PCOS women display both elevated mean LH levels, as well as an elevated frequency of LH pulsatile secretion. The abnormally high LH pulse frequency, reflective of a hyperactive gonadotropin-releasing hormone (GnRH) neural circuit, suggests a neuroendocrine basis to either the etiology or phenotype of PCOS. Several studies in preclinical animal models of PCOS have demonstrated alterations in GnRH neurons and their upstream afferent neuronal circuits. Some rodent PCOS models have demonstrated an increase in GnRH neuron activity that correlates with an increase in stimulatory GABAergic innervation and postsynaptic currents onto GnRH neurons. Additional studies have identified robust increases in hypothalamic levels of kisspeptin, another potent stimulator of GnRH neurons. This review outlines the different brain and neuroendocrine changes in the reproductive axis observed in PCOS animal models, discusses how they might contribute to either the etiology or adult phenotype of PCOS, and considers parallel findings in PCOS women.
Highlights
Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine disorder and a leading cause of infertility, affecting at least 10% of reproductive-age women [1]
There is a greater incidence of PCOS in women with epilepsy [17,18]. This is associated with transient increases in luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin levels [19], which is reflective of altered hypothalamic-pituitary function that might contribute to PCOS
Due to challenges associated with logistics and ethical issues, there has been limited progress in identifying the root causes of PCOS, especially at the level of the brain and pituitary
Summary
Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine disorder and a leading cause of infertility, affecting at least 10% of reproductive-age women [1]. The secretion of GnRH from the brain is itself regulated by a number of upstream neural and endocrine factors that contribute to both the timing and magnitude of GnRH secretion Such regulators include hypothalamic populations of neurons expressing kisspeptin and gamma aminobutyric acid (GABA), amongst others. There is a greater incidence of PCOS in women with epilepsy [17,18] This is associated with transient increases in LH, FSH and prolactin levels [19], which is reflective of altered hypothalamic-pituitary function that might contribute to PCOS. Changes in GABA levels and action might be directly or indirectly modifying the hypothalamus-pituitary-gonadal (HPG) axis, a possibility discussed more in later sections Taken together, these correlative relations point to changes in the neuroendocrine axis as a possible contributing factor to the etiology of PCOS. PCOS research models, and discuss how this may relate to the human PCOS condition
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