{"id":4411895,"date":"2023-02-16T22:15:29","date_gmt":"2023-02-17T03:15:29","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/?p=4411895"},"modified":"2023-03-16T04:42:52","modified_gmt":"2023-03-16T09:42:52","slug":"glucocorticoids-vs-corticosteroids","status":"publish","type":"post","link":"https:\/\/myendoconsult.com\/learn\/glucocorticoids-vs-corticosteroids\/","title":{"rendered":"Glucocorticoids vs Corticosteroids"},"content":{"rendered":"

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Corticosteroids <\/strong>are a class of steroid hormones produced by the adrenal cortex that play diverse physiological roles in the body. They include glucocorticoids, mineralocorticoids, and androgens.<\/p>\n

Glucocorticoids<\/strong> are a family of steroid hormones that are synthesized from the adrenal cortex<\/strong> that play a pivotal role in the treatment of inflammation, cancer, and autoimmune diseases. Furthermore, glucocorticoids play an essential role in the metabolism of fat, protein, and glucose in the body.<\/p>\n

Synthesis of glucocorticoids occurs primarily in the cortex of the adrenal gland alongside dehydro-epi-androsterone (DHEA)<\/strong> and aldosterone (a mineralocorticoid)<\/strong>. DHEA<\/strong> is the precursor of estrogen<\/strong> and testosterone<\/strong>. DHEA, glucocorticoids, and aldosterone are synthesized in the mitochondria by different steroidogenic enzymes. But they share one thing in common \u2013 they are synthesized from cholesterol. Interestingly, various studies have reported extra-adrenal glucocorticoid production<\/strong> in the vasculature, thymus, epithelial barriers, and the brain.<\/p>\n

The medical significance of glucocorticoids arises from their anti-allergic, immune-suppressive, and anti-inflammatory role in the body. It is worth mentioning that the immune-suppressive role of glucocorticoids is pivotal in medical treatment. It is also worth noting that glucocorticoids are not the anabolic steroids used for muscle buildup, but are rather catabolic steroids that trigger the breakdown of peripheral muscle.<\/p>\n

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Cortisol is the essential glucocorticoid in the human body. Its secretion occurs in a diurnal circadian pattern<\/strong>, with the lowest levels released between 12am (midnight) and 4am and the peak levels released around 8am.\u00a0This article will highlight the different types of glucocorticoids and their physiological role in the human body.<\/p>\n

Synthesis & release of glucocorticoids<\/h2>\n

Glucocorticoids (known as corticosterone in rodents and cortisol in humans) are synthesized in the adrenal glands and released in a circadian manner. The release of glucocorticoids occurs in response to stress and physiological cues.1<\/sup><\/p>\n

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Cortisol release is controlled by the hypothalamic-pituitary-adrenal (HPA)<\/strong> axis. Corticotrophin-releasing hormone (CRH) is secreted from the hypothalamus. CRH stimulates then stimulates the production of adrenocorticotrophic hormone (ACTH). ACTH subsequently binds to the melanocortin two receptor<\/strong> \u2013 MC2R<\/strong>, a G protein-coupled receptor<\/strong>. The binding of ACTH to MC2R activates adenylyl cyclase, production of cAMP, and protein kinase A (PKA) activation. PKA modifies the activity of certain transcription factors via phosphorylation. As a result, the modified transcription factors can bind to specific DNA sequences in the nucleus, such as the cAMP response element (CRE), and stimulate the transcription of genes involved in glucocorticoid synthesis, such as the steroidogenic acute regulatory protein (StAR) and cytochrome P450 enzymes (CYP11A1 and CYP17A1). This leads to the increased production and release of glucocorticoids, such as cortisol, from the adrenal gland into the circulation<\/p>\n

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The production of glucocorticoid in zona fasciculata<\/strong> involves 11\u03b2-hydroxylase<\/strong>, 17a-hydroxylase<\/strong>, 21-hydroxylase<\/strong>, and desmolase<\/strong>. The end product is cortisone. Cortisone is the inactive form of cortisol<\/a>. Cortisone is converted in the liver to cortisol. The conversion is facilitated by type 1 hydroxysteroid dehydrogenase<\/strong>. The activated cortisol is bound to cortisol binding protein, a globulin protein (produced by the liver) and released in the blood.2<\/sup> It is important to note that cortisol has the potential to bind to and activate both glucocorticoid<\/strong> and aldosterone receptors <\/strong>under physiological conditions. 11-\u03b2 hydroxysteroid (type II) dehydrogenase <\/strong>prevents the activation of mineralocorticoid receptors by converting cortisol to cortisone (the inert form of cortisol). However, 11\u03b2-hydroxysteroid dehydrogenase becomes saturated when cortisol levels are very high, thus activating mineralocorticoid receptors. This is usually due to treatment with supra-physiologic doses of exogenous glucocorticoids.3<\/sup><\/p>\n

After binding to a glucocorticoid receptor, the cortisol-GR complex is translocated inside the nucleus. The compound alters gene expression and induces various effects on the body cells like white blood cells, fibroblasts, etc.4\u00a0<\/sup>Cortisol has a half-life of 66 minutes under physiological conditions.<\/p>\n