Pathological pulses in PCOS

被引:66
作者
Coyle, Christopher [1 ,2 ]
Campbell, Rebecca E. [1 ,2 ]
机构
[1] Univ Otago, Sch Biomed Sci, Ctr Neuroendocrinol, 270 Great King St, Dunedin 9054, New Zealand
[2] Univ Otago, Sch Biomed Sci, Dept Physiol, 270 Great King St, Dunedin 9054, New Zealand
关键词
Polycystic ovary syndrome; Luteinizing hormone; Androgen; Kisspeptin; GnRH; Pulse generator; GONADOTROPIN-RELEASING-HORMONE; POLYCYSTIC-OVARY-SYNDROME; ANTI-MULLERIAN HORMONE; PRENATAL TESTOSTERONE TREATMENT; HYPOTHALAMIC-PITUITARY AXIS; MESSENGER-RNA EXPRESSION; LUTEINIZING-HORMONE; NEGATIVE FEEDBACK; DIAGNOSTIC-CRITERIA; ANDROGEN PRODUCTION;
D O I
10.1016/j.mce.2019.110561
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine disorder associated with hyperandrogenism and anovulation. Although a spectrum disorder, many women with PCOS exhibit elevated luteinizing hormone (LH) pulse frequency and an elevated LH to follicle stimulating hormone ratio. This aberrant pattern of gonadotrophin signalling drives many of the downstream ovarian features of PCOS, including increased androgen synthesis, and indicates neuroendocrine impairments upstream. Decreased responsiveness to gonadal steroid hormone negative feedback in PCOS patients points toward dysfunction within the gonadotropin-releasing hormone (GnRH) neuronal network in the brain. Excessive androgen exposure during development or over pubertal onset can recapitulate the neuroendocrine pathology of PCOS in pre-clinical models, and these models have been fundamental in beginning to pick apart the specific central mechanisms involved. This mini-review will briefly describe the pathology of PCOS associated with high frequency GnRH/LH pulses and then highlight what is currently known, and yet to be discovered, about the central mechanisms involved.
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页数:10
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