Pituitary control of hepatic steroid metabolism.
Hypophysectomy of male animals has little effect on the hepatic 4-androstene-3,17-dione (androstenedione) metabolism except at the kinetic level where changes in the apparent Km of the 16 alpha- and 7 alpha-hydroxylases are seen. On the other hand, hypophysectomy of female animals leads to a "masculinization" of hepatic androstenedione metabolism, following the changes seen in Vmax of the respective enzymes probably due to the removal of the source of "feminizing factor" thought to maintain the female-type metabolism in the liver. There seems to be a temporal dissociation of the effects on the various enzymes indicating different cellular control mechanisms for these enzymes. Oestrogen treatment of male rats causes "feminization" of the hepatic androstenedione metabolism. The time study shows an initial increase in 17-hydroxysteroid oxidoreductase, 6 beta- and 16 alpha-hydroxylase activities followed by a decrease to the levels of females. This biphasic effect is possibly due to an initial direct effect of the oestrogen on the liver followed by an indirect effect via the hypothalamo-pituitary system. The changes in enzyme activity noted are related to changes in Vmax of the respective enzymes although changes in apparent Km are also seen.
D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D013006:Growth Hormone / Q000097:blood; D007016:Hypophysectomy; D007700:Kinetics; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000201:enzymology*; D011388:Prolactin / Q000097:blood; D051381:Rats; D012737:Sex Factors; D013250:Steroid Hydroxylases / Q000378:metabolism*
D004958:Estradiol; D011388:Prolactin; D013006:Growth Hormone; D015067:17-Hydroxysteroid Dehydrogenases; D013250:Steroid Hydroxylases