Thyroid Hormone Regulates Rat Pituitary Insulin-Like Growth Factor-I Receptors

Abstract

As we previously obtained evidence that insulin-like growth factor-I (IGF-I) inhibits T3-induced GH secretion and GH mRNA expression without affecting basal GH secretion in thyroidectomized rat pituitary cells grown in hypothyroid medium, we examined changes in IGF-I receptors in the pituitary gland, as induced by thyroid hormone. Thyroidectomized rats and a quantitative receptor autoradiographic method were used. The density of [125I]IGF-I-binding sites in the anterior pituitary gland decreased 4 weeks after thyroidectomy; that is a significant decrease in the number of the receptors compared to findings in control rats (P less than 0.01). The affinity (Kd) remained unchanged. There were no changes in binding parameters in the ventroposterior thalamic nucleus in the brain, renal cortex, and liver parenchyma. The ip administration of T4 once a day (48 micrograms/kg) for 1-2 weeks compensated for the decrease in the binding capacity of [125I]IGF-I-binding sites to that of the control values (P less than 0.01). We propose that IGF-I receptors in the anterior pituitary gland may be regulated by thyroid hormone.

Effects of iodine deficiency on insulin‐like growth factor‐I, insulin‐like growth factor‐binding protein‐3 levels and height attainment in malnourished children

“…In this study, IGFBP-3 levels, notably in the 4-10 years age group, were highly significantly correlated with T4. This is consistent with the fact that thyroid hormone has been shown to regulate the expression of IGF-I (Nanto-Salonen et al, 1993) and its receptors (Matsuo et al, 1990;King et al, 1988) and that in vitro, T3 has been shown to directly stimulate GH3 cells to produce IGFBP-3 (Ceda et al, 1992). The low levels of IGF-I and IGFBP-3 seen especially in the children from Sinderut and Pos Lanai could thus possibly be due to the low serum T4 levels.…”

Body dimensions and thyroid hormone levels in premenopausal and postmenopausal women from Austria

“…The thyroid hormones also have an anabolic effect; hypothyroid animals and humans have fewer muscle cells than normal conspecifics (Cheek et al, 1965). Triiodothyronine, either by itself or in interaction with somatotropin, stimulates the secretion of the growth factor somatomedin-C, which is essential for normal growth and development (Phillips and Unterman, 1984;Binoux et al, 1985;Ikeda et al, 1989Ikeda et al, , 1990Wolf et al, 1989;Matuso et al, 1990).…”

Effects of growth hormone and thyroxine on kidney insulin-like growth factor-I and renal growth in hypophysectomized rats

“…Thyroid hormones stimulate transcription of the GH and IGF-I genes in pituitary-derived cells (Melmed & Yamashita, 1986;Fagin et al 1989), enhance the release of IGF-I from fetal mouse hypo¬ thalamus (Binoux et al 1985) and increase the num¬ ber of IGF-I receptors on anterior pituitary but not renal cells in thyroidectomized rats (Matsuo et al 1990). Our present study in hypophysectomized ani¬ mals suggests that, although thyroid hormones in isol¬ ation stimulate kidney growth by an alternative pathway to the GH/IGF-I axis, when given along with GH, they produce tissue-selective additive effects with the GH/IGF-I axis in peripheral tissues.…”