The normal prostate gland is created intrauterine (“inside the uterus“) at 12 weeks of gestation, but then remains rudimentary until it continues to develop at puberty under the influence of androgens.
Endogenous prostate-related hormones are produced 90% in the testis and 10% in the adrenal cortex.
Testosterone is the most important androgen. It is produced in the Leydig cells of the testis under the influence of luteinizing hormone (LH) from the pituitary gland. The secretion (release) of LH, in turn, is regulated by LH-releasing hormone (LHRH) from the hypothalamus (section of the diencephalon). Testosterone has a negative feedback effect in the hypothalamus and thus slows down the further secretion of LHRH, LH and testosterone.
The most important androgen of the adrenal gland is dehydroepiandrosterone (DHEA). Its formation is stimulated by adrenocorticotropic hormone (ACTH). Stimulation of ACTH release occurs via corticotropin-releasing hormone (CRH).
In the prostate, both androgens are metabolized (metabolized) by 5-α-reductase to dihydrotestosterone (DHT). DHT is three to five times more potent than testosterone itself. In the nuclear membrane, DHT is bound to the androgen receptor, this leads via several intermediate steps to the release of important growth factors such as epidermal growth factor (EGF) or platelet-derived growth factor (PdGF).
The normal development and function of the prostate depends on a balanced homeostasis (flow equilibrium) between cell death and cell replacement. Androgens are a prerequisite for this. Both chemical and surgical castration (removal of both testes) results in a rapid increase in the rate of cell death (apoptosis). Conversely, the supply of androgens results in restoration of normal prostate architecture and function.
In addition to testosterone, other hormones have now been identified that have been linked to prostate growth. For example, FSH can stimulate prostate cell growth in vitro (“in the test tube”), and FSH receptors have also been identified in the prostate. This suggests an autocrine-paracrine growth regulatory circuit in the prostate.
