The synthesis of hormones necessary for sexual differentiation and reproduction is carried out by the testes and ovaries, also known as gonads. Gonadotropin-releasing hormone, a single hypothalamic-releasing factor, stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. Similar to ACTH, LH and FSH bind to surface receptors and lead to an increase in cAMP. Testosterone production is stimulated by LH in the testes, while estrogen and progesterone production in the ovaries is stimulated by LH as well. FSH, on the other hand, regulates the growth of ovarian follicles and stimulates testicular spermatogenesis.

The mechanism behind the action of steroid hormones involves diffusion of each hormone across the plasma membrane of its target cell. It then binds to a specific cytosolic or nuclear receptor. The resulting receptor-ligand complexes accumulate in the nucleus, dimerize, and bind to specific regulatory DNA sequences known as hormone response elements (HRE), along with coactivator proteins. This leads to increased transcription of targeted genes, ensuring coordinated regulation of these genes. The promoter or enhancer elements of genes responsive to a specific steroid hormone contain an HRE. Hormone-receptor complexes can also inhibit transcription when associated with corepressors. Upon hormone binding, the receptor undergoes a conformational change that exposes its DNA-binding domain, allowing interaction with the appropriate DNA sequence through a zinc finger motif. Receptors for steroid hormones, thyroid hormone, retinoic acid, and 1,25-dihydroxycholecalciferol (vitamin D) are part of a superfamily of structurally related gene regulators that function similarly.

Metabolism of steroid hormones involves their conversion into inactive metabolic excretion products in the liver. This process includes the reduction of unsaturated bonds and the addition of hydroxyl groups. The resulting structures are made more soluble by conjugation with glucuronic acid or sulfate. These conjugated metabolites are water-soluble and do not require protein carriers. They are eliminated from the body through feces and urine.

In summary, the testes and ovaries synthesize hormones necessary for sexual differentiation and reproduction. Gonadotropin-releasing hormone stimulates the release of LH and FSH from the anterior pituitary, which in turn stimulate hormone production in the gonads. The action of steroid hormones involves binding to specific receptors, leading to increased transcription of targeted genes through interaction with hormone response elements. Metabolism of steroid hormones occurs in the liver, resulting in the formation of conjugated metabolites that are eliminated from the body.
The testes and ovaries (gonads) synthesize hormones necessary for sexual differentiation and reproduction. A single hypothalamic-releasing factor, gonadotropin-releasing hormone, stimulates the anterior pituitary to release the glycoproteins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Like ACTH, LH and FSH bind to surface receptors and cause an increase in cAMP. LH stimulates the testes to produce testosterone and the ovaries to produce estrogens and progesterone (see Fig. 18.27). FSH regulates the growth of ovarian follicles and stimulates testicular spermatogenesis.
D. Mechanism
Each steroid hormone diffuses across the plasma membrane of its target cell and binds to a specific cytosolic or nuclear receptor. These receptor–ligand complexes accumulate in the nucleus, dimerize, and bind to specific regulatory DNA sequences (hormone response elements [HRE]) in association with coactivator proteins, thereby causing increased transcription of targeted genes (Fig. 18.28). An HRE is found in the promoter or an enhancer element (see p. 440) for genes that respond to a specific steroid hormone, thus insuring coordinated regulation of these genes. Hormone–receptor complexes can also inhibit transcription in association with corepressors. [Note: The binding of a hormone to its receptor causes a conformational change in the receptor that uncovers its DNA-binding domain, allowing the complex to interact through a zinc finger motif with the appropriate DNA sequence. Receptors for the steroid hormones, plus those for thyroid hormone, retinoic acid (see p. 386), and 1,25-dihydroxycholecalciferol (vitamin D; see p. 390), are members of a superfamily of structurally related gene regulators that function in a similar way.]
E. Further metabolism
Steroid hormones are generally converted into inactive metabolic excretion products in the liver. Reactions include reduction of unsaturated bonds and the introduction of additional hydroxyl groups. The resulting structures are made more soluble by conjugation with glucuronic acid or sulfate (from 3′phosphoadenosyl-5′-phosphosulfate; see p. 162). These conjugated metabolites are fairly water soluble and do not need protein carriers. They are eliminated in feces and urine.
VIII. CHAPTER SUMMARY