**5.1 Pituitary hormones**

The pituitary secretes several hormones that stimulate the release of steroid hormones. In this process, two key hormones are the ACTH and LH, and their release is pulsating. Higher cortisol, progesterone, testosterone, and estradiol levels in serum are observed minutes after each ACTH or LH pulse. By acting on the expression of several genes, ACTH and LH stimulate the synthesis of enzymes participating in the conversion of cholesterol to steroid hormones, a process that can take hours or even days. The rapid increase in steroid hormone concentrations after the injection of ACTH or LH cannot be explained by the synthesis of enzymes participating in steroid hormones synthesis and release. Based on several studies, it has been proposed that the rapid increase in steroid hormones levels is mediated by a c-AMP action resulting in StAR synthesis, one of the proteins carrying the cholesterol to the mitochondria, the first step in steroid hormones synthesis (Auchus & Miller, 2000).

The first step in the acute response to hormonal stimulation for steroid biosynthesis is the delivery of cholesterol from the outer to the inner mitochondrial membrane; a process that depends on *de novo* StAR protein synthesis and phosphorylation. LH and ACTH stimulate the synthesis of StAR by increasing cAMP levels and its phosphorylation rate (Luo et al., 2010).

LH plays a dual role in regulating P-450 enzymes participating in the synthesis of steroid hormones. Following the initial stimulation synthesis of the enzyme, LH exerts a down regulation on the synthesis of granulosa-specific CYP19A1 and theca-specific CYP17A1 transcripts and lowers the abundance of HSD3B1 transcripts (Nimz et al., 2010).

In female rabbits, hyperprolactinemia inhibits the peripheral and ovarian venous progesterone and 20 alpha-hydroxypregn-4-en-3-one (20 alpha-OHP) levels increase stimulated by human chorionic gonadotropin (hCG), without causing changes in the estradiol, androstenedione and testosterone levels (Lin et al., 1987).
