Influence of recombinant chicken prolactin on thyroid hormone metabolism in the chick embryo

The influence of a recombinant chicken prolactin (rcPRL) preparation on thyroid function was studied in 18- and 19-day-old chicken embryos. Displacement studies on hepatic microsomes indicate that this preparation does not compete with radiolabeled chicken growth hormone (cGH) for hepatic GH-receptor binding. In a first series of experiments rcPRL or immunoaffinity-purified cGH was injected intravenously in 19-day-old chicken embryos. After 2 hr, cGH increased plasma T3 in a dose-dependent way by inhibiting hepatic inner ring type III deiodination (IRD-III) and consequently T3 degradation. Outer ring deiodination (ORD-I) was not influenced confirming previous results. The rcPRL preparation (2 and 10 microg) did not influence plasma T3, but depressed T4 and raised hepatic IRD-III activity simultaneously, whereas no influence on hepatic ORD-I activity could be found. In a second experiment on 18-day-old embryos, it could be demonstrated that the effect of 2.5 microg cGH on plasma T3 and liver IRD-III lasted up to 6 hr after injection, whereas 2.5 microg cPRL affected plasma T4 and liver IRD-III up to 2 hr. Both rcPRL and cGH depressed rT3 up to 6 hr, whereas an injection of rcPRL, but not of cGH, elevated plasma concentrations of corticosterone. These results indicate that prolactin may have a role, together with GH, in controlling peripheral thyroid hormone metabolism.