[Lotus]

Does prostate produce cortisteriods?

Great question Pom, the adrenals produce glucocorticoids from the HPA (pituitary) axis, if that's what you mean. I did say complicated right? Lol. But this action itself isn't significant enough to flip the switch of without outside (pharma) help.

There is a hrt therapy (I forgot who, sorry), that uses another process that simply bypasses all (most) of androgen production -gonadotropin-releasing hormone analogue (and I will let wiki explain this one lol)
http://wikipedia.org/wiki/Gonadotropin-releasing_hormone_analogue

A gonadotropin-releasing hormone analogue (GnRH analogue or analog), also known as a luteinizing hormone releasing hormone agonist (LHRH agonist) or LHRH analogue is a synthetic peptide drug modeled after the human hypothalamic gonadotropin-releasing hormone (GnRH). A GnRH analogue is designed to interact with the GnRH receptorand modify the release of pituitary gonadotropins FSH and LH for therapeutic purposes. Shortly after the discovery of GnRH by Nobel laureates Guillemin and Schally researchers tried to modify the GnRH decapeptide with the intent to synthesize stimulating and blocking variants.

Hormones share cholesterol as a common precursor. In consequence, the first step in steroidogenesis is cholesterol uptake or synthesis. Cells that produce steroid hormones provide themselves with cholesterol in various ways. Their main source is dietary cholesterol transported in the blood as LDL, which enters the cells through receptor-mediated endocytosis, although endogenous synthesis in the endoplasmic reticulum is sufficient when LDL levels are abnormally low as represented in people with abetalipoproteinemia (a genetic disorder of intestinal lipid absorption).[3] In lysosomes, cholesterol is separated from the proteic component of LDL and then stored within cell membranes or bound with proteins.[26]

The initial part of conversion of cholesterol into steroid hormones involves a number of enzymes of the cytochrome P450 family that are located in the inner membrane of mitochondria. Transport of cholesterol from the outer to the inner membrane is facilitated by steroidogenic acute regulatory protein (StAR) and is the rate-limiting step of steroid synthesis.[26] The functional zonation of the adrenal cortex is determined by the presence of distinct enzymes in each particular layer, explaining how the different layers produce unique hormones from a common precursor.[3]

The first enzymatic step in the production of all steroid hormones is cleavage of the cholesterol side chain, a reaction that forms pregnenolone as a product and is catalyzed by the enzyme P450scc, also known as cholesterol desmolase. After the production of pregnenolone, specific enzymes of each cortical layer further modify it. Enzymes involved in this process include both mitochondrial and cytoplasmic P450s and hydroxysteroid dehydrogenases (HSDs). Usually a number of intermediate steps in which pregnenolone is modified several times are required to form the functional hormones.[4] Enzymes that catalyze reactions in these metabolic pathways are involved in a number of endocrine diseases. For example, the most common form of congenital adrenal hyperplasia develops as a result of deficiency of 21-hydroxylase, an enzyme involved in an intermediate step of cortisol production.[27]


Glucocorticoids are under the regulatory influence of the hypothalamus-pituitary-adrenal (HPA) axis. Glucocorticoid synthesis is stimulated by adrenocorticotropic hormone (ACTH), a hormone of the anterior pituitary. In turn, production of ACTH is stimulated by the presence of corticotropin-releasing hormone (CRH), which is released by neurons of the hypothalamus. ACTH acts on the adrenal cells first by increasing the levels of StAR within the cells, and then of all steroidogenic P450 enzymes. The HPA axis is an example of a negative feedback system, in which cortisol itself acts as a direct inhibitor of both CRH and ACTH synthesis. The HPA-axis also interacts with the immune system through increased secretion of ACTH at the presence of certain molecules of the inflammatory response.[3]

Mineralocorticoid secretion is regulated mainly by the renin–angiotensin–aldosterone system (RAAS), the concentration of potassium, and ACTH to a lesser extent.[3] Sensors of blood pressure in the juxtaglomerular apparatus of the kidneys release the enzyme renin into the blood, which starts a cascade of reactions that lead to formation of angiotensin II. Angiotensin receptors in cells of the zona glomerulosa recognize the substance, and upon binding they stimulate the release of aldosterone.[28]

http://en.m.wikipedia.org/wiki/Adrenal_gland#Corticosteroid_production