RETRACTED: LKB1 suppresses androgen synthesis in a mouse model of hyperandrogenism via IGF‐1 signaling

Polycystic ovary syndrome ( PCOS ) is a major cause of anovulatory sterility in women, and most PCOS patients exhibit hyperandrogenism ( HA ). Liver kinase b1 ( LKB 1) is a tumor suppressor that has recently been reported to be involved in PCOS . However, the mechanism by which LKB 1 affects HA has not previously been elucidated. We report here that ovarian LKB 1 levels are significantly decreased in a female mouse model of HA . Moreover, we report that LKB 1 expression is inhibited by elevated androgens via activation of androgen receptors. In addition, LKB 1 treatment was observed to suppress androgen synthesis in theca cells and promote estrogen production in granulosa cells by regulating steroidogenic enzyme expression. As expected, LKB 1 knockdown inhibited estrogen levels and enhanced androgen levels, and LKB 1‐transgenic mice were protected against HA . The effect of LKB 1 appears to be mediated via IGF ‐1 signaling. In summary, we describe here a key role for LKB 1 in controlling sex hormone levels.