Adrenocorticotropic hormone
Adrenocorticotropic hormone (ACTH or corticotropin) is a polypeptide hormone (a chain of 10-100 amino acids) synthesised from a large glycoprotein called pro-opiomelanocortin, or POMC. ACTH is secreted from the anterior lobe of the pituitary gland in response to the hormone corticotropin-releasing hormone (CRH), which is released by the hypothalamus into the hypothalamic- hypophyseal portal system (modified portion of the circulation that transports neurohormones from the hypothalamus directly to the anterior pituitary).
Structure
ACTH consists of 39 amino acids, the first 13 of which (counting from the N-terminus) may be cleaved to form α-MSH. (This common structure is one reason that patients with hypocortisolism/Addison's disease, in which ACTH levels are elevated, often present with hyperpigmentation/excessively tanned skin.)
The half-life of ACTH in human blood is about 10 minutes.
Function
ACTH acts through the stimulation of cell surface ACTH receptors, which are primarily located on the adrenocortical cells in the cortex (outer portion) of the adrenal glands. Stimulation of the cortex of the adrenal gland boosts the synthesis of several secretes. The inner most layer of the cortex, the zona reticularis, secretes sex steroids (mostly androgens). The middle portion, the zona fasciculata, secretes mainly glucocorticoids such as cortisol, but also some mineralcorticoids. The zona glomerulosa, the outer layer of the cortex, releases only aldosterone.
With the secretion of ACTH, the hormones lipotropin, melanocyte-stimulating hormone (MSH), β-endorphin and met-enkephalin are also released. ACTH secretion is related to the circadian rhythm in many organisms with secretion peaking during the morning hours. The secretion of ACTH is controlled by CRH, circadian rhythm, and through negative feedback from blood levels of cortisol and other secretes from the adrenal cortex.
Pathologies
Abnormal secretion of ACTH or an abnormal response to the hormone can lead to various pathologies. A pituitary tumor, which may secrete ACTH autonomously, can lead the adrenal gland to oversecrete cortisol, causing Cushing's disease. Such a tumor is not subject to normal regulation of ACTH secretion. An unusual response, or lack of response, by the adrenal cortex to ACTH can lead to hyposecretion of various secretes and can contribute to disease's such as hypocortisolism/ Addison's disease.
See also
- Addison's disease
- Cushing's syndrome
- ectopic tumor
- Hypothalamic-Pituitary-adrenal axis
- Nelson syndrome
| Hormones and endocrine glands - edit |
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Hypothalamus: GnRH - TRH - CRH - GHRH - somatostatin - dopamine | Posterior pituitary: vasopressin - oxytocin | Anterior pituitary: GH - ACTH - TSH - LH - FSH - prolactin - MSH - endorphins - lipotropin Thyroid: T3 and T4 - calcitonin | Parathyroid: PTH | Adrenal medulla: epinephrine - norepinephrine | Adrenal cortex: aldosterone - cortisol - DHEA | Pancreas: glucagon- insulin - somatostatin | Ovary: estradiol - progesterone - inhibin - activin | Testis: testosterone - AMH - inhibin | Pineal gland: melatonin | Kidney: renin - EPO - calcitriol - prostaglandin | Heart atrium: ANP Stomach: gastrin | Duodenum: CCK - GIP - secretin - motilin - VIP | Ileum: enteroglucagon | Liver: IGF-1 Placenta: hCG - HPL - estrogen - progesterone Adipose tissue: leptin, adiponectin Target-derived NGF, BDNF, NT-3 |
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