The influence of endogenous GH levels on peripheral monodeiodination activity has been investigated in growing chickens at the age of 4 weeks, when they normally show no T3 increase after GH injection. Injection of anti-GH serum decreased plasma T3 and increased plasma T4. Three d and 1 week after hypophysectomy, plasma T3 was also markedly decreased, while T4 was only slightly affected, hepatic 5'D-I activity showed a transient decrease, but 5D-III activity was highly increased, as were the number of hepatic GH receptor sites. Injection of GH in hypophysectomized chickens decreased 5D-III activity and increased plasma T3. GH receptor-deficient dwarf chickens had decreased plasma T3 and increased plasma T4 and hepatic 5'D-I and 5D-III activities compared to their normally-growing siblings. GH administration could only affect T3 and 5D-III in the non-dwarf siblings, which showed higher basal 5D-III activity compared to the non-responsive age-matched chickens of die Hisex strain used in the other experiments. It can be concluded that endogenous GH is an important factor in the control of plasma T3 levels in growing chickens due to its influence on the activity of the T3-degrading type III deiodinase. The effectiveness of exogenous GH administration to acutely increase plasma T3 probably depends on the balance between the injected dose and the endogenous GH concentration, the hepatic GH receptor availability and the hepatic type III deiodinase level.