DIFFERENTIAL STIMULATORY EFFECT OF THYROID-HORMONE ON GROWTH-HORMONE SYNTHESIS AND ESTROGEN ON PROLACTIN SYNTHESIS DUE TO ACCUMULATION OF SPECIFIC MESSENGER RIBONUCLEIC-ACIDS

Thyroid and steroid hormones bind to chromatin-associated nuclear protein receptors which appear to be hormone specific and are believed to mediate the action of these hormones through synthesis of mRNA. The purpose of this investigation was to test the hypothesis of hormonal control through regulation of specific gene expression. Rat GH and PRL were chosen as a model, since previous work has indicated that the synthesis of these hormones is regulated by thyroid hormone and estrogen, respectively. Male rats were kept intact (N) or were thyroidectomized (Tx) and treated with estradiol (N + E or Tx + E) or replaced with T4, (Tx + T4). GH and PRL synthesis was determined in quarter pituitaries by the in vitro incorporation of [3H]leucine into specific immunoprecipitates. GH and PRL mRNA activity was measured by cell-free translation of total RNA extracted from the remaining pituitary tissue. Tx suppressed both GH synthesis and mRNA activity to 2.8% and 1.4% of the level in N rats and was not affected by treatment with estrogen (Tx + E). One week of T4 replacement in Tx rats normalized GH synthesis and mRNA activity. In contrast, 1 week of estrogen treatment increased PRL synthesis, to 286% and 332% the respective control levels of N and Tx rats. Although administration of estrogens for 4 months increased PRL synthesis and the mRNA activity to 14- and 13-fold the basal level, respectively, treatment for only 1 week increased PRL synthesis by only 3.3-fold when the PRL mRNA activity was already 11.2-fold the basal level. This lag in the induction of PRL synthesis, producing the observed discrepancy with the PRL mRNA activity measured in the same tissue, may be related to a similar observation reported for the induction of vitellogenin. None of the hypotheses suggested to explain this phenomenon of latency have been confirmed. Our data indicate that thyroid hormone and estrogens regulate the synthesis of GH and PRL, respectively. However, because of our inability to determine the effect of these hormones on the proliferation of specific pituitary cell types, it remains unclear whether their effect on the accumulation of specific mRNAs is mediated through the control of the expression of specific genes. © 1979 by The Endocrine Society.