Testosterone metabolism in normal males and male cirrhotics.
The following physiopathological mechanisms for the abnormalities of testosterone metabolism observed in cirrhotic patients may be postulated: 1. The decreased testosterone secretion has a primary testicular origin; it seems probable that, as a result of direct toxicity the 17-beta-reductase is inhibited, resulting in decrease of testosterone and an increase of androstenedione. 2. The hypothalamic-pituitary function is nearly normal in cirrhotics. Basal level of LH and FSH are often slightly elevated, indicating a normal reactivity of the pituitary. 3. The conversion of androgens to oestrogens (androstenedione to oestrone) which occurs essentially extrahepatically, is increaed in cirrhosis.
D000273:Adipose Tissue / Q000378:metabolism; D000735:Androstenedione / Q000032:analysis; D003687:Dehydroepiandrosterone / Q000032:analysis; D006801:Humans; D008099:Liver / Q000378:metabolism; D008103:Liver Cirrhosis / Q000378:metabolism*; D008297:Male; D008657:Metabolic Clearance Rate; D011944:Receptors, Androgen; D013737:Testis / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism*
D011944:Receptors, Androgen; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone