Anti-ACTH antibody [SPM501]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Adrenocorticotropic hormone (ACTH) also known as corticotropin is a peptide hormone secreted by the pituitary gland. It is a 39-amino acid polypeptide with a molecular mass of approximately 4540 Da. ACTH is primarily expressed in the anterior pituitary gland and smaller amounts can be found in the central nervous system. Its production and secretion are tightly regulated by corticotropin-releasing hormone (CRH) through a feedback mechanism involving the hypothalamic-pituitary-adrenal (HPA) axis.

Biological function summary

Adrenocorticotropic hormone stimulates the adrenal cortex to produce and release glucocorticoids especially cortisol. ACTH is not part of a larger complex but acts as a singular hormone in its pathway. The hormone also influences the expression of certain enzymes important for steroid biosynthesis. In addition to its role in the adrenal cortex ACTH can mildly interact with melanocortin receptors on adipose tissues contributing to lipolysis and inflammatory processes.

Pathways

Adrenocorticotropic hormone functions in the HPA axis one of the body's key stress response systems. The hormone also involves in the regulation of the corticosteroid biosynthesis pathway. The primary protein it interacts with in these processes is cortisol which in turn regulates many physiological processes including immune response and metabolism. ACTH and cortisol form a feedback loop where elevated cortisol levels inhibit the release of both CRH and ACTH.

Associated diseases and disorders

Increased or decreased levels of adrenocorticotropic hormone can result in disorders such as Cushing's disease and Addison's disease. Cushing's disease is characterized by overproduction of ACTH often due to pituitary adenomas leading to excess cortisol production. Conversely in Addison’s disease inadequate ACTH or adrenal cortex dysfunction leads to insufficient cortisol production. Both conditions highlight the disrupted feedback relationship between ACTH and cortisol resulting in significant clinical symptoms that require careful management.