**4.2 3β-Hydroxysteroid dehydrogenase/∆5-4-isomerases**

3β-Hydroxysteroid dehydrogenase/Δ5-4-isomerases (3β-HSDs) are located at the microsomal fraction, and are expressed in the adrenal cortex and in steroidogenic cells of the

Hormonal and Neural Mechanisms Regulating Hormone Steroids Secretion 7

synthesis. The stimulating actions of FSH on aromatase are potentiated by insulin-like growth factor-1 (IGF-1), because IGF-I stimulates the capacity of granulosa cells to respond

FSH stimulates the synthesis of cAMP, which in turn acts as an intracellular messenger mediating FSH stimulation of aromatase expression, leading to the activation of the cAMPdependent protein kinase A (PKA) which is cAMP-dependent (Stocco, 2008). FSH stimulates the mRNA for LH receptor synthesis, explaining why LH is the main aromatase

The regulation of steroid hormones synthesis is mediated by hormones secreted by the

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 &

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.,

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

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

The adipose tissue secretes several adipose-derived polypeptidic hormones. Together, adipose-derived polypeptidic hormones receive the name of adipokines. Adipokines act locally and distally through autocrine, paracrine and endocrine effects (Ronti et al., 2006), and participate in the regulation of appetite and metabolic processes. Experimental studies show that some adipokines play a role regulating steroid hormones secretion by different organs.

transcripts and lowers the abundance of HSD3B1 transcripts (Nimz et al., 2010).

estradiol, androstenedione and testosterone levels (Lin et al., 1987).

pituitary, thyroid, adipose tissue, neuropeptides, adrenals, ovaries and testicles.

to FSH (Stocco 2008).

**5. Hormonal signals** 

**5.1 Pituitary hormones** 

Miller, 2000).

**5.2 Adipose tissue hormones** 

2010).

inductor before ovulation (Boon et al., 2010).

gonads. The expression of 3β-HSDs is enhanced by ACTH and LH. These isomerases catalyze the formation of Δ4-3-ketosteroids from A5-3β-hydroxysteroids, an obligate step in the biosynthesis of progestins, androgens, estrogens, mineralocorticoids and glucocorticoids. 3β-HSDs catalyze the dehydrogenation of the 3B-equatorial hydroxyl group and the subsequent isomerization of the olefinic bond to yield the A4 3-ketone structure; converting pregnenolone into progesterone, l7α-hydroxypregnenolone into 17αhydroxyprogesterone, and dehydroepiandrosterone into A4.

Protein kinase A signaling activators (forskolin, dibutyrylcAMP) increase the synthesis of dehydroepiandrosterone and A4, as well as the levels of 3β-HSD and P-450c17 mRNA transcripts. Activation of the protein kinase C pathway by phorbol ester treatment also elevates 3β-HSD mRNA levels and lowers P-450cl17 mRNA levels (Auchus & Miller. 2000).
