Insulin-like growth factor I enhances gonadotropin-releasing hormone-stimulated luteinizing hormone release from bovine anterior pituitary cells

Abstract

The role of insulin-like growth factor I (IGF-I) in the release of luteinizing hormone (LH) is unclear in ruminants. In the present study, the effects of IGF-I on the release of LH stimulated by gonadotropin-releasing hormone (GnRH) were examined in primary cultures of bovine anterior pituitary (AP) cells, and the interaction between estradiol-17β (E 2) and IGF-I was characterized. GnRH(100 nM)-stimulated LH release from the cultured cells was increased ( P<0.05) 12, 24 and 36 h after addition of IGF-I (250 ng/ml), with a maximum at 12 h (48.4 ng/ml media versus 35.4 ng/ml media in controls). IGF-I at concentrations of 25, 250 and 500 ng/ml increased the release by 18.7, 24.2 and 28.9%, respectively ( P<0.05), when compared with controls (37.2 ng/ml media). E 2 (10 nM), IGF-I (250 ng/ml) and combined treatment of E 2 plus IGF-I also induced significant increases in LH release ( P<0.05). The amounts of LH release after treatment with E 2 alone was 37.3% greater than with IGF-I alone (39.0 ng/ml media versus 28.4 ng/ml media) ( P<0.05). When E 2 and IGF-I were added together (45.6 ng/ml media), the release of LH was significantly greater than with either E 2 alone or IGF-I alone ( P<0.05). E 2 (10 nM) significantly ( P<0.05) increased the amount of GnRH bound to the cells by 51.6% when compared with controls, however, IGF-I (250 ng/ml) failed to increase GnRH binding. These results show that IGF-I enhances GnRH-stimulated LH release without changing the number of GnRH receptors in cattle, and IGF-I interacts with E 2 to increase the response to GnRH.