Glucocorticoids: Difference between revisions

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Glucocorticoids are a type of [[Steroid hormone|steroid hormone]] that are produced in the [[Adrenal cortex|adrenal cortex]].
Glucocorticoids (e.g. [[Cortisol|Cortisol]]) are a type of [[Steroid hormone|steroid hormone]] that are one of the two main corticosteroids produced in the [[Adrenal cortex|adrenal cortex]] of the [[Adrenal gland|adrenal gland]] that is situated just above the [[Kidneys|kidneys]]. The other major corticosteroids are mineralocorticoids. Corticosteroids are [[Catabolic steroids|catabolic steroids]] meaning that they break down stored resources in the body through their [[Metabolic|metabolic]] effects (whereas [[Anabolic steroids|anabolic steroids]] would build up muscle mass)<ref>Lorraine I. McKay, PhD and John A. Cidlowski, PhD. - Physiologic and Pharmacologic Effects of Corticosteroids - Available at:https://www.ncbi.nlm.nih.gov/books/NBK13780/ - Accessed: 03/12/16</ref>.
 
These [[Hormones|hormones]] have their major effects on [[Metabolism|metabolism]] (such as the metabolism of [[Carbohydrates|carbohydrates]], [[Lipids|lipids]] and [[Protein|protein]]) and have anti-inflammatory effects. [[ANTI-INFLAMMATORY DRUGS|Glucocorticoid drugs]] have similar anti-inflammatory effects to the natural steroid hormone<ref>Stephen Liou (29/06/10) - Glucocorticoids - Available at: http://web.stanford.edu/group/hopes/cgi-bin/hopes_test/glucocorticoids/#what-are-glucocorticoids - Accessed 03/12/16</ref>.
 
Glucocorticoids have an affect on a number of different processes that result in maintaining the normal [[Glucose|glucose]] concentrations in blood. This includes the increase in [[Glucose|glucose]] production in cells such as the [[Liver|liver]], and the breakdown of [[Fat|fat]] in [[Adipose tissue|adipose tissues]]. As well as inhibiting the process of storing [[Fat|fats]] and [[Glucose|glucose]] within cells.
 
Glucocorticoids are able to cross the [[Cell membrane|cell membrane]] and interact with [[Intracellular receptors|intracellular receptors]] in order to enter the [[Nucleus|nucleus]] of cells acting as [[Transcription factor|transcription factors]] so that it can have a direct effect on the [[DNA|DNA]] to change [[MRNA|mRNA]] synthesis thereby producing different proteins or, increasing or decreasing the number of proteins produced. They can use this effect to suppress proteins that cause [[Inflammation|inflammation]]<ref>Barnes PJ. (June 1998) - Anti-inflammatory actions of glucocorticoids: molecular mechanisms - Available at: https://www.ncbi.nlm.nih.gov/pubmed/9854452 - Accessed on: 3/12/16</ref>. Glucocorticoids can also activate lipocortins enzymes which help to inhibit an [[Enzyme|enzyme]] that releases arachidonic acid from [[Cell membrane|cell membranes]] (this acid can be converted in several substances some of which cause [[Inflammation|inflammation]]). Although the [[Inflammatory process|inflammatory process]] is necessary to protect the body from damage and disease by releasing the required cells and mediators to combat infections and foreign substances. When [[Inflammation|inflammation]] lasts too long it can be deadly to the body and leads to [[Chronic inflammation|chronic inflammation]].
 
A chronic excess of glucocorticoids (e.g. from oral steroid therapy) which causes a loss of the normal feedback function and can lead to [[Cushing sydrome|Cushing's syndrome]].  
 
=== References ===
 
<references />

Latest revision as of 21:05, 5 December 2017

Glucocorticoids (e.g. Cortisol) are a type of steroid hormone that are one of the two main corticosteroids produced in the adrenal cortex of the adrenal gland that is situated just above the kidneys. The other major corticosteroids are mineralocorticoids. Corticosteroids are catabolic steroids meaning that they break down stored resources in the body through their metabolic effects (whereas anabolic steroids would build up muscle mass)[1].

These hormones have their major effects on metabolism (such as the metabolism of carbohydrates, lipids and protein) and have anti-inflammatory effects. Glucocorticoid drugs have similar anti-inflammatory effects to the natural steroid hormone[2].

Glucocorticoids have an affect on a number of different processes that result in maintaining the normal glucose concentrations in blood. This includes the increase in glucose production in cells such as the liver, and the breakdown of fat in adipose tissues. As well as inhibiting the process of storing fats and glucose within cells.

Glucocorticoids are able to cross the cell membrane and interact with intracellular receptors in order to enter the nucleus of cells acting as transcription factors so that it can have a direct effect on the DNA to change mRNA synthesis thereby producing different proteins or, increasing or decreasing the number of proteins produced. They can use this effect to suppress proteins that cause inflammation[3]. Glucocorticoids can also activate lipocortins enzymes which help to inhibit an enzyme that releases arachidonic acid from cell membranes (this acid can be converted in several substances some of which cause inflammation). Although the inflammatory process is necessary to protect the body from damage and disease by releasing the required cells and mediators to combat infections and foreign substances. When inflammation lasts too long it can be deadly to the body and leads to chronic inflammation.

A chronic excess of glucocorticoids (e.g. from oral steroid therapy) which causes a loss of the normal feedback function and can lead to Cushing's syndrome.

References

  1. Lorraine I. McKay, PhD and John A. Cidlowski, PhD. - Physiologic and Pharmacologic Effects of Corticosteroids - Available at:https://www.ncbi.nlm.nih.gov/books/NBK13780/ - Accessed: 03/12/16
  2. Stephen Liou (29/06/10) - Glucocorticoids - Available at: http://web.stanford.edu/group/hopes/cgi-bin/hopes_test/glucocorticoids/#what-are-glucocorticoids - Accessed 03/12/16
  3. Barnes PJ. (June 1998) - Anti-inflammatory actions of glucocorticoids: molecular mechanisms - Available at: https://www.ncbi.nlm.nih.gov/pubmed/9854452 - Accessed on: 3/12/16