Ovarian Actions of Estrogen Receptor-β

An Update

Ann E. Drummond, Ph.D.; Peter J. Fuller, B.Med.Sci., M.B.B.S., Ph.D., F.R.A.C.P.


Semin Reprod Med. 2012;30(1):32-38. 

In This Article

Polycystic Ovarian Syndrome

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by anovulation, elevated levels of androgen, hirsutism, and insulin resistance.[64,65] Folliculogenesis is arrested at the antral stage of development, and it is the accumulation of these follicles that gives the ovary its characteristic morphology of a necklace-like pattern of follicles in the periphery. Because estrogen has been shown to be essential for folliculogenesis beyond the antral stage, it is perhaps not surprising that ERβ mRNA and protein are reduced in granulosa cells and theca cells from PCOS patients.[11,66] We hypothesized that changes in the ratio of ERβ τo ERα may result in abnormal follicular development. Similarly, in a rodent model of PCOS, levels of ERβ protein were decreased in the granulosa layers of cystic follicles.[67] Idiopathic ovulatory dysfunction has been found to be associated with a G/A (1730) polymorphism in ERβ.[2] Given that ovulatory dysfunction is a key feature of PCOS, one group investigated a cohort of PCOS patients to determine if there was an association with this polymorphism.[68] They reported significant differences in the genotype distribution and allelic frequencies between controls and PCOS patients that supported a correlation with the G/A polymorphism.[68] To date, the underlying mechanism has not been established.


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