The administration of glucocorticoids fails to induce tyrosine aminotransferase activity in fetal rat liver in utero but causes a marked increase in the activity of this enzyme in postnatal rats. In adult animals, this increase has been shown to be the result of the production of enhanced amounts of mRNA for tyrosine aminotransferase, leading to an increase in the rate of synthesis of the enzyme. The lack of steroid response in utero is not due to an impairment in uptake of the hormone by fetal liver, nor is it due to a lack of glucocorticoid receptors, as both cytoplasmic and nuclear receptors have been detected in fetal liver. In studies with cultured fetal hepatocytes, dexamethasone is able to induce the enzyme but the presence of insulin prevents this induction at a post-transcriptional step. It is therefore proposed, that glucocorticoids are active at the transcriptional level in fetal liver but that a high concentration of insulin inhibits some post-transcriptional process, thus preventing the synthesis of tyrosine aminotransferase (TAT).
|Number of pages||10|
|Journal||Advances in the Biosciences|
|Publication status||Published - 1 Dec 1980|