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The site of action of gonadal hormones in the regulation of hepatic steroid metabolism was investigated by measuring the effects of (i) implantation of oestradiol into the pituitary gland or anterior hypothalamus of males and (ii) subcutaneous injection of a synthetic androgen in deafferentated male and female rats. The hepatic responses measured in vitro were 5α-reduction, and 6β- and 16α-hydroxylation of androstenedione.
After intrapituitary or intrahypothalamic implantation of oestradiol, 5α-reductase activity increased and 6β- and 16α-hydroxylase activity decreased in males relative to the enzyme activities of cholesterol-implanted animals, indicating a feminizing effect of the oestrogen. This effect could not be accomplished by subcutaneous injection of the same oestrogen preparation.
Deafferentation had no effect on hepatic steroid metabolism in females, but caused a feminization in males. In addition, subcutaneous treatment of intact females with the synthetic androgen caused masculinization of hepatic steroid metabolism, but was without effect in deafferentated animals. Treatment with synthetic androgens had no effect on the hepatic steroid metabolism in deafferentated male animals. Subcutaneous injection of a potent synthetic progestagen had little effect on hepatic steroid metabolism in intact females.
It is concluded that oestrogen feminizes hepatic steroid metabolism by an action at the hypothalamic-pituitary level and that an intact hypothalamic-pituitary axis is required for the masculinizing action of the synthetic androgen on hepatic steroid metabolism. It is possible that the site of action of androgens is in the anterior hypothalamus or in adjacent areas of the brain.
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The metabolism of 4-[4-14C]androstene-3,17-dione in the microsomal fraction of livers from male and female rats was investigated after hypothalamic deafferentation at two levels. It was found that frontal deafferentation at the retrochiasmatic level caused a complete 'feminization' of hepatic steroid metabolism in the male rat but was without effect in the female animal. Transection rostral to the suprachiasmatic nuclei was without effect in both sexes. A complete transition from male to female hepatic steroid metabolism after retrochiasmatic deafferentation was reached on day 4 after the operation and persisted for at least 10 weeks. The present results, taken together with previous investigations, indicate that the release of a 'feminizing' factor from the pituitary gland of the male rat is inhibited by a factor produced in, or transported through, the periventricular anterior hypothalamic region including the suprachiasmatic area. No effect on the hepatic steroid metabolism was observed after blinding of the rats suggesting that a diurnal rhythm is not essential to this control mechanism.
