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Endocrine Abstracts (2021) 73 S13.2 | DOI: 10.1530/endoabs.73.S13.2

1Institute of Reproductive & Developmental Biology, Imperial College London; 2Laboratory of Reproductive Biology, The Juliane Marie Centre for Women, Children and Reproduction, Copenhagen University Hospital, University of Copenhagen


The luteinising hormone/chorionic gonadotropin receptor (LHCGR) plays an essential role in ovarian follicular function, mediating the action of LH on theca cell steroidogenesis and, in the preovulatory follicle, on granulosa cell (GC) steroid production and the ovulatory cascade. Following ovulation, LH (and CG) are responsible for maintenance and function of the corpus luteum. Arrested antral follicle development in PCOS is characterised by premature responsiveness of GCs to LH and recent studies in our laboratory have indicated that LHCGR mRNA is increased in GCs of small, human antral follicles (hSAFs). A similarly increased gene expression of LHCGR was observed in granulosa-lutein cells (GLCs) from PCOS women. Several previous studies point to the interaction of LH with members of the TGF-β family. TGF-β’s, activin, inhibins and AMH have all been implicated in modulating LH action in both theca and granulosa cells. In our recent study we found that aberrant expression of LHCGR in GCs of hSAFs in PCOS, was associated with increased expression of inhibin A, but not of inhibin B, AMH, AMH receptor 2 (AMHR2) or follistatin. Nevertheless, there are functional studies that implicate AMH in abnormalities of gonadotropin-induced steroidogenesis in women with PCOS and there remains considerable scope for further investigation in attempting to understand what role the interaction between gonadotropins and members of the TGF-β family has to play in the mechanism of anovulation in PCOS.

Volume 73

European Congress of Endocrinology 2021

Online
22 May 2021 - 26 May 2021

European Society of Endocrinology 

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