Kortisolina

Kortisolina, or cortisol, is a steroid hormone produced by the adrenal cortex and serves as the principal glucocorticoid in humans. It plays a central role in the body’s response to stress, metabolism, and immune regulation.

Synthesis occurs in the zona fasciculata of the adrenal cortex under the control of the hypothalamic-pituitary-adrenal (HPA) axis. Kortisolina production is stimulated by adrenocorticotropic hormone (ACTH) released from the pituitary in response to corticotropin-releasing hormone (CRH) from the hypothalamus. It exhibits a pronounced circadian rhythm, with higher levels in the morning and a nadir at night, and it rises in response to acute stress.

Physiologically, kortisolina promotes gluconeogenesis in the liver, mobilizes amino acids from muscle, and stimulates lipolysis. It helps regulate blood glucose, maintains vascular tone, and suppresses inflammatory and immune responses. Kortisolina acts via the intracellular glucocorticoid receptor and has permissive effects on other tissues and hormones, thereby coordinating metabolism and immune function during stress.

Circulation and metabolism: most kortisolina is bound to corticosteroid-binding globulin (CBG) and albumin; only the free fraction is biologically active. It is primarily metabolized in the liver and excreted as inactive metabolites in the urine.

Clinical relevance: chronically high kortisolina levels cause Cushing syndrome; deficiency leads to adrenal insufficiency (Addison disease). Diagnosis uses morning serum cortisol, salivary cortisol, or 24-hour urinary free cortisol, and may include dexamethasone suppression testing. Long-term exogenous glucocorticoid therapy can produce iatrogenic hypercortisolism and requires careful management.