Abstract

Cytosolic sulfating activities of 4-pregnen-11 beta, 17 alpha, 21-triol-3,20-dione (cortisol) to the 21-sulfate were 4 to 5 times higher in livers of female than male adult rats. The activity was decreased by administration of testosterone propionate (TP) to ovariectomized, but not to intact, female rats. In male rats, the rate of cortisol sulfation was elevated by neonatal castration and was restored in part by the administration of TP to the castrated rats. In addition, the sulfating activity in adult male rats was increased by the treatment with estradiol benzoate. Hypophysectomy almost completely decreased cytosolic cortisol-sulfating activity in male rats. The activity in hypophysectomized male rats was not increased by the treatment with hydrocortisone, TP, estradiol benzoate, or somatomedin C but was restored by the intermittent injection of human growth hormone (hGH). Further, the continuous infusion of hGH, to mimic the female secretory pattern, increased more efficiently the rate of cortisol sulfation. Hypophysectomy of female rats also decreased, but not completely, the sulfating activity. Treatment of female hypophysectomized rats intermittently with hGH had no appreciable effect, but the continuous infusion increased the activity effectively. The involvement of pituitary growth hormone in the hepatic cortisol sulfation was also supported by the experiment using neonatally glutamate-treated rats and by the observation of developmental changes in the cortisol-sulfating activity. These results indicate that pituitary growth hormone is one of the major factors regulating hepatic levels of cortisol sulfation in rats and that the higher activity in the female than the male is due mainly to the difference in the secretory pattern of growth hormone in the adult animals.