Adrenocorticotropic hormone (ACTH, also known as corticotropin) is a tropic hormone and an important player in the HPA axis. It is produced and released by the anterior pituitary gland. ACTH acts on its target organ, the adrenal glands, by stimulating the release of cortisol.
Structure and Function[edit | edit source]
There is a two-step process for the release of ACTH. First, the hypothalamus releases corticotropin-releasing hormone (CRH) through the hypophyseal portal system to stimulate the anterior pituitary gland. Corticotropin-releasing hormone is normally released in response to biological stress, and is a part of the general stress response. The anterior pituitary gland responds by releasing ACTH, targeting the adrenal glands (specifically the adrenal cortex). ACTH stimulates the production and secretion of glucocorticoid steroid hormones from the adrenal cortex. Cortisol is one of the principal hormones secreted, and is released into the bloodstream where it helps convert fats and proteins into glucose, and has an anti-inflammatory effect. ACTH also affects the production of aldosterone in the adrenal cortex. Aldosterone facilitates sodium reabsorption and potassium secretion in the kidneys. Thus, ACTH is important in glucose, fat, and protein metabolism, the immune system’s response, and maintenance of blood pressure.
Dysfunction[edit | edit source]
Pathophysiology of ACTH arises from dysfunction of the pituitary, the adrenal glands, or ectopic secretion. If the pituitary is hypo- or hyper-functioning, there will be a respective decrease or increase in ACTH secretion. If the adrenal glands are hypo- or hyper-functioning, the response to ACTH may be muted or exaggerated. Ectopic secretion describes the secretion of ACTH from an abnormal source, such as a tumor, such that normal regulatory pathways do not control such levels.
Pathophysiologies associated with ACTH dysregulation include:
ME[edit | edit source]
As ACTH is a major hormone in the HPA axis, ACTH may be related to myalgic encephalomyelitis (ME) because HPA axis dysregulation has been associated with ME. However, studies in this area have found a wide range in results; a 2007 review of HPA function in ME found that about half of all studies indicated HPA hypofunction in ME, whereas the other half of the studies did not find differences in ACTH within HPA function between ME and controls. This could be partly explained by how some patients report higher levels of ACTH and cortisol early in the disease, with depleted/lower levels as the disease progresses.
See also[edit | edit source]
Learn more[edit | edit source]
- Anatomy and Physiology | ACTH
References[edit | edit source]
- "Adrenocorticotropic Hormone". www.vivo.colostate.edu. Retrieved Oct 25, 2018.
- "ACTH". labtestsonline.org. Retrieved Oct 25, 2018.
- Allen, Mary J.; Sharma, Sandeep (2018). "Physiology, Adrenocorticotropic Hormone (ACTH)". Treasure Island (FL): StatPearls Publishing. PMID 29763207.
- Van Den Eede, Filip; Moorkens, Greta; Van Houdenhove, Boudewijn; Cosyns, Paul; Claes, Stephan J. (2007). "Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome". Neuropsychobiology. 55 (2): 112–120. doi:10.1159/000104468. ISSN 0302-282X.
Myalgic encephalomyelitis (ME) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.