<unk>  is caused by dysregulation of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), otherwise known as<unk>  reductase, a bi-directional enzyme, which catalyzes the interconversion of<unk>  to cortisol in the presence of NADH as a co-factor. If levels of NADH are low, the enzyme catalyses the reverse reaction, from cortisol to<unk> , using NAD+ as a co-factor. Cortisol is a glucocorticoid that plays a variety of roles in many different biochemical pathways, including, but not limited to: gluconeogenesis, suppressing immune system responses and carbohydrate metabolism. One of the symptoms of<unk>  is hyperandrogenism, resulting from activation of the Hypothalamic–pituitary–adrenal axis. The deficiency has been known to exhibit symptoms of other disorders such as Polycystic Ovary Syndrome in women.<unk>  alone has been reported in fewer than ten cases in total, all but one case were women. Elevated activity of 11β-HSD1 can lead to obesity or Type II Diabetes, because of the role of cortisol in carbohydrate metabolism and gluconeogenesis.
Cortisone reductase deficiency
Isolated 17,20-lyase deficiency
17β-Hydroxysteroid dehydrogenase III deficiency
5α-Reductase 2 deficiency
Aromatase deficiency
Gonadotropin-releasing hormone insensitivity
Androgen-induced hermaphroditism
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency