Modulation of pituitary insulin-like growth factor-I bindings in rats bearing somatomammotrophic tumors.

To clarify the hormonal regulation of pituitary insulin-like growth factor-I (IGF-I) bindings, we examined the continuous effect of growth hormone (GH) on [125I] IGF-I binding sites, using rats bearing transplantable GH-secreting rat pituitary tumor cells. A total of 24 female Wistar-Furth rats (4-week old) was divided into four groups (n = 6). The first group rats were control (C). The second group rats were injected subcutaneously with 3 x 10(6) GH3 pituitary tumor cells (GH). The third group rats were thyroidectomized (Tx) and the fourth were dual-treated (GHTx). The brain, pituitary gland, liver, and kidney were immediately subjected to quantitative receptor autoradiography after a 4-week treatment period. Using kinetic experiments, GH rats had higher Bmax values of specific [125I] IGF-I binding sites in the anterior pituitary gland and Tx rats had lower Bmax values than control rats. Two-way analysis of variance among the 4 groups was examined. The effects of both GH and Tx treatment on [125I] IGF-I binding Bmax were observed only in the anterior pituitary gland and not in the other tissues examined. There were no differences in the Kd values of the binding sites. These data indicate that continuous GH excess selectively up-regulates the number of pituitary IGF-I binding sites in vivo, and that this may play a role in feedback regulation of the GH-IGF-I axis.