Copyright 2018 . All rights reserved. DISCLAIMER: By printing, downloading, or using you agree to our full terms. Review the full terms at the following URL: http:///Terms-of-Service . If you do not agree to the full terms, do not use the information. We are only publishers of this material, not authors. Information may have errors or be outdated. The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. Statements made pertaining to the properties or functions of nutritional supplements have not been evaluated by the Food and Drug Administration. If you have a medical problem or symptoms, consult your physician. User assumes all risk of use, damage, or injury. You agree that we have no liability for any damages. We are not liable for any consequential, incidental, indirect, or special damages. You indemnify us for claims caused by you.
The mineralocorticoid pathway starts with 21-hydroxylation of progesterone to form deoxycorticosterone (DOC). The enzyme in this reaction, 21-hydroxylase, is encoded by the CYP21 gene. 11 , 12 Deoxycorticosterone is then converted to corticosterone through the action of 11β-hydroxylase. There are two distinct 11β-hydroxylase isoenzymes, both of which are encoded by two genes, CYP11B1 and CYP11B2 . 13 Corticosterone is hydroxylated at carbon 18 to form 18-hydroxycorticosterone, which is transformed to aldosterone by removal of two hydrogens (oxidation) at carbon 18. These two reactions are catalyzed by 18-hydroxylase and 18-hydroxysteroid dehydrogenase, respectively, which are encoded by the same gene, CYP11B2 . Transcription of CYP11B1 is regulated primarily by ACTH, whereas angiotensin II regulates CYP11B2 transcription. 14 , 15 Similarly, the glucocorticoid pathway begins with 17α-hydroxyprogesterone, which is converted to deoxycortisol and subsequently to cortisol by 21-hydroxylase and 11β-hydroxylase, respectively, in the same manner as the conversion of progesterone to corticosterone. A deficiency of 21-hydroxylase, 11β-hydroxylase, or 3β-HSD in the adrenals may result in congenital adrenal hyperplasia and female pseudohermaphroditism, manifested as a masculinized female fetus.