Cortisol / cortisone ratio indicates activity of HSD11B2 activity and assessment of tissue specific concentrations of cortisol, which normally cannot be measured without a biopsy.
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Cortisol is a hormone produced by the adrenal glands that plays a crucial role in various physiological processes, including metabolism, immune response, and stress regulation. It is known as a glucocorticoid hormone. To be active in the body, cortisol must bind to specific receptors, such as the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR).
One of the key enzymes involved in cortisol metabolism is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). This enzyme is primarily responsible for converting active cortisol to its inactive form, cortisone, by oxidizing cortisol. The conversion of cortisol to cortisone is essential to protect MRs from being occupied by cortisol, as the MRs have equal affinity for cortisol and aldosterone, another hormone involved in regulating blood pressure and fluid balance.
The role of 11β-HSD2 in maintaining proper mineralocorticoid signaling is crucial, as excessive activation of MRs by cortisol can lead to a condition known as apparent mineralocorticoid excess (AME). AME is characterized by hypertension (high blood pressure) along with hypokalemia (low potassium levels), metabolic alkalosis, low renin activity, and reduced aldosterone levels. These symptoms arise when 11β-HSD2 is impaired, leading to excessive cortisol activating MRs and mimicking the effects of aldosterone on the kidneys and other tissues.
Inherited mutations in the 11β-HSD2 gene can cause AME, and it typically follows an autosomal recessive pattern of inheritance. Additionally, AME can also be acquired through the ingestion of substances that act as competitive inhibitors of 11β-HSD2, such as liquorice.
Besides its role in mineralocorticoid signaling, 11β-HSD2 also impacts the availability of cortisol to bind to glucocorticoid receptors in various peripheral tissues. The activity of this enzyme is believed to play a role in the pathogenesis of diverse human diseases, including hypertension, intrauterine growth retardation, apparent cortisone reductase deficiency, insulin resistance, and visceral obesity. Therefore, modulating the activity of 11β-HSD isozymes presents a potential therapeutic approach to managing certain human diseases while avoiding the consequences of systemic glucocorticoid excess or deficiency.
Overall, 11β-HSD2 is a critical enzyme in cortisol metabolism and its proper functioning is essential to maintain hormonal balance and prevent harmful effects of excessive cortisol on mineralocorticoid receptors.
Cortisol/Cortione 11B-HSD II
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