Contradictory Evidence Concerning the “Universal” Role of Growth Hormone in the Regulation of the Enzyme Activities of Hepatic Steroid Metabolism

Summary

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 3α-hydroxysteroid dehydrogenase (3α-HSDH), microsomal 3α-HSDH and microsomal 5α-reductase which could be reversed by continuous infusion of human growth hormone (hGH). However, one activity did not conform to this pattern : cytoplasmic 17β-HSDH activity reacted to hypophysectomy with a “feminization” and was completely unaffected by hGH infusion. Moreover, microsomal 3α-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.

Key words

Growth hormone - Steroid metabolism - PRL