type species | type | NADH dehydrogenase | Type (biology) | Diabetes mellitus type 1 | Type O Negative | Diabetes mellitus type 2 | Volkswagen Type 2 | Type I and type II errors | Lactate dehydrogenase | Type 56 assault rifle | type (biology) | Type 38 | Bugatti Type 57 | Type II supernova | Type Directors Club | Type 38 rifle | type genus | Type 59 | Type 45 destroyer | Jaguar S-Type | Handley Page Type O | Geranylgeranyltransferase type 1 | Blood type | Word (data type) | urban-type settlement | Type species | Type O' Negative | Type 21 frigate | Type 212 submarine |
Mineralocorticoid manifestations of severe 11β-hydroxylase deficient CAH can be biphasic, changing from deficiency (salt-wasting) in early infancy to excess (hypertension) in childhood and adult life.
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Because 11β-hydroxylase activity is not necessary in the production of sex steroids (androgens and estrogens), the hyperplastic adrenal cortex produces excessive amounts of DHEA, androstenedione, and especially testosterone.
Finally, DHEA is thought to regulate a handful of other proteins via indirect, genomic mechanisms, including the enzymes P4502C11 and 11β-HSD1—the latter of which is essential for the biosynthesis of the glucocorticoids such as cortisol and has been suggested to be involved in the antiglucocorticoid effects of DHEA—and the carrier IGFBP1.
Maneb interferes with glucocorticoid metabolism by inhibiting the activity of the enzyme 11β-hydroxysteroid dehydrogenase type 2 which converts cortisol to cortisone.