EFFECTS OF THYROID HORMONES ON LIVER BINDING SITES FOR HUMAN GROWTH HORMONE, AS STUDIED IN THE RAT

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Abstract
Several weeks after thyroidectomy (.hivin.T), female rats stopped growing, and their pituitary GH [growth hormone] content decreased to less than 2-3% of the values found for age-matched controls (C). The liver membranes of such animals were explored with human GH (hGH). In the severely hypothyroid .hivin.T rat, the number, but not the affinity, of the lactogenic binding sites was markedly reduced. Treatment of these rats for 3 wk with 1.75 .mu.g T4 [thyroxine] or 0.5 .mu.g T3 [triiodothyronine]/100 g body wt/day restored growth, increased pituitary GH content and restored the number of liver lactogenic binding sites practically to normal. As regards the lactogenic binding sites, similar results were obtained when the severly hypothyroid rats were treated with a much lower T4 dose (0.2 .mu.g/100 per day); this dose was clearly growth promoting and restored both the low circulating GH levels and the pituitary PRL [prolactin] content of the severely hypothyroid rat to normal. The changes in plasma PRL were not clear. The lactogenic binding sites on liver membranes from rats which were both thyroidectomized and hypophysectomized decreased in number. Treatment with 0.5 .mu.g T3/100 g per day for 30 days (but not for 12 days) resulted in an increased number of lactogenic binding sites, though it did not affect growth or the undetectable plasma GH levels. The effect on the lactogenic binding sites was less marked than in .hivin.T rats with an intact pituitary. Minute amounts of thyroid hormones are apparently needed for maintenance of liver lactogenic binding sites; it is possible that this not only occurs through mechanism(s) which involve the pituitary, but also through others which do not. The possible role of these receptors in growth processes is not yet clearly understood.