Journal
STEROIDS
Volume 77, Issue 4, Pages 332-337Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.steroids.2011.12.007
Keywords
Polycystic ovarian syndrome; Gonadotropin releasing hormone; Obesity; Puberty; Hyperandrogenemia; Neuroendocrine
Funding
- General Clinical Research Center [M01 RR00847]
- Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institute of Health [U54 HD28934, F32 HD066855]
- National Institute for Diabetes and Digestive and Kidney Diseases [T32 DK07646]
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Polycystic ovarian syndrome (PCOS) is a common disorder characterized by ovulatory dysfunction and hyperandrogenemia (HA). Neuroendocrine abnormalities including increased gonadotropin-releasing hormone (GnRH) pulse frequency, increased luteinizing hormone (LH) pulsatility, and relatively decreased follicle stimulating hormone contribute to its pathogenesis. HA reduces inhibition of GnRH pulse frequency by progesterone, causing rapid LH pulse secretion and increasing ovarian androgen production. The origins of persistently rapid GnRH secretion are unknown but appear to evolve during puberty. Obese girls are at risk for HA and develop increased LH pulse frequency with elevated mean LH by late puberty. However, even early pubertal girls with HA have increased LH pulsatility and enhanced daytime LH pulse secretion, indicating the abnormalities may begin early in puberty. Decreasing sensitivity to progesterone may regulate normal maturation of LH secretion, potentially related to normally increasing levels of testosterone during puberty. This change in sensitivity may become exaggerated in girls with HA. Many girls with HA-especially those with hyperinsulinemia-do not exhibit normal LH pulse sensitivity to progesterone inhibition. Thus, HA may adversely affect LH pulse regulation during pubertal maturation leading to persistent HA and the development of PCOS. (C) 2011 Elsevier Ltd. All rights reserved.
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