steroidogenic

Steroidogenic is an adjective describing processes, tissues, or enzymes involved in the biosynthesis of steroid hormones. Steroidogenesis refers to the production of steroids from cholesterol and occurs primarily in the adrenal cortex, gonads, and placenta, with contributing activity in the brain and adipose tissue.

The biosynthetic pathway begins with cholesterol, imported into mitochondria by the steroidogenic acute regulatory protein (StAR) and converted to pregnenolone by the cholesterol side-chain cleavage enzyme (CYP11A1, P450scc). From pregnenolone, further enzymatic steps—catalyzed by 3β-hydroxysteroid dehydrogenase (3β-HSD), 17α-hydroxylase/17,20-lyase (CYP17A1), 21-hydroxylase (CYP21A2), and 11β-hydroxylase (CYP11B1), among others—produce glucocorticoids (cortisol), mineralocorticoids (aldosterone), androgens, and estrogens. Aromatase (CYP19A1) converts androgens to estrogens in certain tissues.

The main steroidogenic tissues are the adrenal cortex (zona glomerulosa producing aldosterone; zona fasciculata producing cortisol; zona reticularis producing androgens), the gonads (Leydig cells synthesize testosterone; thecal and granulosa cells participate in ovarian steroidogenesis), and the placenta. Brain and other tissues also express steroidogenic enzymes, contributing to local steroid production.

Regulation involves endocrine and local controls. Adrenal steroidogenesis is stimulated by ACTH; gonadal steroid production is driven by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Cholesterol availability and nutritional status influence synthesis, while cortisol exerts negative feedback on CRH and ACTH.

Clinical relevance includes disorders of steroidogenesis caused by enzyme deficiencies, such as congenital adrenal hyperplasia due to 21-hydroxylase or 11β-hydroxylase deficiency, leading to impaired cortisol synthesis and excess androgen production. Aromatase deficiency affects sex steroid balance.