Lax E R, Bergheim E, Peetz A, Schriefers H
Exp Clin Endocrinol. 1986 Jul;87(2):142-8. doi: 10.1055/s-0029-1210535.
Recent publications suggest that the sexual dimorphism observed in the activities of enzymes involved in drug and steroid metabolism in rat liver are due to sex-specific differences in the rate of growth hormone release. In this paper we set out to demonstrate that this hypothesis cannot be generalized, but has its limitations. Prepuberal hypophysectomy led to the expected "masculinization" of the activities of cytoplasmic 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSDH), microsomal 3 alpha-HSDH and microsomal 5 alpha-reductase which could be reversed by continuous infusion of human growth hormone (hGH). However, one activity did not conform to this pattern: cytoplasmic 17 beta-HSDH activity reacted to hypophysectomy with a "feminization" and was completely unaffected by hGH infusion. Moreover, microsomal 3 alpha-HSDH in hypophysectomized rats was "feminized" as efficiently by infusion of ovine prolactin (oPRL) as by hGH. Ablation of the pituitary caused loss of measurable cytoplasmic receptor oestrogen concentrations. The inability of either hypophyseal hormone to cause consistent and significant elevation of oestrogen receptor concentrations is probably due to the early age at which the animals were hypophysectomized.
最近的出版物表明，在大鼠肝脏中参与药物和类固醇代谢的酶活性中观察到的性别二态性是由于生长激素释放速率的性别特异性差异。在本文中，我们着手证明这一假设不能一概而论，而是有其局限性。青春期前垂体切除导致细胞质3α-羟基类固醇脱氢酶（3α-HSDH）、微粒体3α-HSDH和微粒体5α-还原酶活性出现预期的“男性化”，这可以通过持续输注人生长激素（hGH）来逆转。然而，有一种活性不符合这种模式：细胞质17β-HSDH活性对垂体切除的反应是“女性化”，并且完全不受hGH输注的影响。此外，垂体切除大鼠中的微粒体3α-HSDH通过输注羊催乳素（oPRL）与通过hGH一样有效地“女性化”。垂体切除导致可测量的细胞质受体雌激素浓度丧失。两种垂体激素都无法导致雌激素受体浓度持续且显著升高，这可能是由于动物进行垂体切除时的年龄较小。
