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Cortisol 

     latin: cortex 

From Wikipedia, the free encyclopedia

Cortisol is a corticosteroid hormone produced by the adrenal gland (in the Zona fasciculata of the adrenal cortex). It is often referred to as the "stress hormone" as it is involved in response to stress. It increases blood pressure and blood sugar, and reduces immune responses. In pharmacology, the synthetic form of cortisol is referred to as hydrocortisone, and is used to treat allergies and inflammation, and to supplement natural cortisol when its production is too low.

Immune system
Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor. Cortisol has a negative feedback effect on interleukin-1[28] which must be especially useful in combating diseases, such as the endotoxin bacteria, that gain an advantage by forcing the hypothalamus to secrete a hormone called CRH. The suppressor cells are not affected by GRMF, so that the effective set point for the immune cells may be even higher than the set point for physiological processes. It reflects leukocyte redistribution to lymph nodes, bone marrow, and skin. Acute administration of corticosterone (the endogenous Type I and Type II receptor agonist), or RU28362 (a specific Type II receptor agonist), to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are not affected by cortisol.

Cortisone was first discovered by the American chemist Edward Calvin Kendall while a researcher at the Mayo Clinic. He won the 1950 Nobel Prize for Physiology or Medicine along with Philip S. Hench and Tadeus Reichstein for the discovery of adrenal cortex hormones, their structures, and functions. Cortisone was first produced commercially by Merck & Co..

Cortisone is one of several end products of a process called steroidogenesis. This process starts with the synthesis of cholesterol which then proceeds through a series of modifications in the adrenal gland (suprarenal) to become any one of many steroid hormones. One end product of this pathway is cortisol. For cortisol to be released from the adrenal gland a cascade of signaling occurs. Corticotropin releasing hormone released from the hypothalamus stimulates corticotrophs in the anterior pituitary to release ACTH which relays the signal to the adrenal cortex. Here, the zona fasiculata and zona reticularis in response to ACTH secrete glucocorticoids, in particular cortisol. In the peripheral tissues cortisol is converted to cortisone by an enzyme called 11-beta-steroid dehydrogenase. Cortisol has much greater glucocorticoid activity than cortisone and thus cortisone can be considered an inactive metabolite of cortisol. However 11-beta-steroid dehydrogenase can catalyze the reverse reaction as well and thus cortisone is also the inactive precursor molecule of the active hormone cortisol. Cortisone is activated through hydrogenation of the 11-keto-group and is thus sometimes referred to as hydrocortisone.

Cortisol, a glucocorticoid, and adrenaline are the main hormones released by the body as a reaction to stress. They elevate blood pressure and prepare the body for a fight or flight response.

Cortisone is sometimes used as a drug to treat a variety of ailments. It can be administered intravenously or cutaneously.

One of cortisone's effects on the body, and a potentially harmful side effect when administered clinically, is the suppression of the immune system. This could be the explanation for the apparent correlation between high stress and sickness. The suppression of the immune system may be important in the treatment of inflammatory conditions such as severe IgE-mediated allergies.

Cortisone is less powerful than a similar steroid cortisol. Cortisol is responsible for 95% of the effects of the glucocorticosteroids while cortisone is about 4 or 5%. Corticosterone is even less important. Cortisol decreases the uptake of glucose by cells and increases glucose release by the liver. This may cause hyperglycemia in a well-fed state but can maintain blood glucose levels in (stressful) fasting states.

 

 

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