Abstract: LH is postulated to regulate exactly the androgen biosynthesis in ovarian theca-cells. LH plays its roles by numerous downstream pathways, including conventional pathways like cAMP-PKA-CREB, PKA-ERK, Ras-Raf-MEK-ERK and PI3K-Akt. LH can stimulate adenylate cyclase（AC）-independed phospholipase C-inositol phosphate （PLC-IP） signaling in ovulatory-size follicles, by which LH induces the differentiation response of granulosa cells. Those classical pathways like Wnt and mTORC1 are related to the androgen biosynthesis in ovaries. The conventional pathways and above classical pathways such as Wnt signaling could act in concert to regulate the ovarian steroidogenesis though the complicated crosstalk. SET protein as a transcriptional regulating factor is widely expressed in various tissues and mediates diverse biological processes. It was recently found that a specific, SET-initiated and PP2A-mediated pathway would lead to the increased lyase activity of P450c17 and the increased testosterone production in ovarian theca cells, which maybe contribute to clarify the hyperandrogenism of polycystic ovarian syndrome（PCOS）. It is important to clarify the pathways involved in the androgen biosynthesis in ovarian theca cells and the hyperandrogenism of PCOS for the treatment of those androgen-related diseases. This review focused on the LH-inducing pathways in regulating steroidogenesis in ovarian theca-cells.

Key words: Luteinizing hormone, Androgens, Receptors, LH, Ovary