Oxo steroid reductase

Bile acids, in particular chenodeoxycholic acid (CDCA) and cholic acid (CA), can regulate the expression of genes involved in their synthesis, thereby, creating a feed-back loop. The elucidation of this regulatory pathway came about as a consequence of the isolation of a class of receptors called the farnesoid X receptors, FXRs . The FXRs belong to the superfamily of nuclear receptors that includes the steroid/thyroid hormone receptor family as well as the liver X receptors (LXRs) , retinoid X receptors (RXRs), and the peroxisome proliferator-activated receptors (PPARs) .

The second isoenzyme of 5α reductase is deficient in the classic intersex condition ( pseudovaginal perineoscrotal hypospadias ), or 5α-reductase deficiency . It was first discovered in indigenous cultures of Papua, New Guinea , where children were born with feminine genitalia in the absence of endogenous DHT during pregnancy, but with the surge of testosterone during adolescence, changed to males at puberty. Because of this change at puberty, the condition is also sometimes called " guevedoche ." [24] There is a range of external appearance that has been described of external genitalia at birth, with varying degrees of virilization.

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Oxo steroid reductase

oxo steroid reductase


oxo steroid reductaseoxo steroid reductaseoxo steroid reductaseoxo steroid reductaseoxo steroid reductase