Skett P
Biochem J. 1978 Sep 15;174(3):753-60. doi: 10.1042/bj1740753.
Hypophysectomy of male animals has little effect on the hepatic androst-4-ene,3,17-dione (androstenedione) metabolism, except for possible changes in the kinetics of the 16alpha-and 7alpha-hydroxylases. On the other hand, hypophysectomy of female animals leads to a "masculinization" of hepatic androstenedione metabolism, following the changes seen in Vmax. of the enzymes involved, probably due to the removal of the source of "feminizing factor" thought to maintain the "female" type of 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-hydroxy steroid oxidoreductase and 6beta- and 16alpha-hydroxylase activities, followed by a decrease to the values in females. This biphasic effect is possibly due to an initial direct effect via the hypothalamo-pituitary system.
切除雄性动物的垂体对肝脏雄甾-4-烯-3,17-二酮(雄烯二酮)代谢影响很小,除了16α-和7α-羟化酶的动力学可能发生变化。另一方面,切除雌性动物的垂体导致肝脏雄烯二酮代谢出现“男性化”,这是由于参与其中的酶的Vmax发生变化所致,可能是因为去除了被认为维持肝脏“女性”代谢类型的“女性化因子”来源。对各种酶的影响似乎存在时间上的分离,表明这些酶有不同的细胞控制机制。用雌激素处理雄性大鼠会导致肝脏雄烯二酮代谢“女性化”。时间研究表明,17-羟类固醇氧化还原酶以及6β-和16α-羟化酶活性最初会增加,随后降至雌性大鼠的水平。这种双相效应可能是由于最初通过下丘脑-垂体系统产生的直接作用。