Effect of administration of growth hormone on plasma and intracellular levels of thyroxine and tri-iodothyronine in thyroidectomized thyroxine-treated rats

We have studied the effects of the administration of GH on plasma levels and peripheral production of tri-iodothyronine (T₃) from thyroxine (T₄) in thyroidectomized male Wistar rats given a continuous i.v. infusion of T₄ (1 μg/ 100 g body weight per day) and GH (120 μg per day) for 3 weeks. Tracer doses of ¹³¹I-labelled T₃ and ¹²⁵I-labelled T₄ were added to the infusion. At isotopic equilibrium (10 days after the addition of ¹²⁵I-labelled T₄) the rats were bled and perfused. The plasma appearance rate for T₃ was higher (10.6 ± 1.3 vs 8.4 ± 2.8 pmol/h per 100 g body weight, P = 0.05) and plasma TSH was lower (246 ± 24 vs 470 ± 135 pmol/l, P < 0.01) in GH-treated rats. The amount of T₃ in liver (12.3 ± 2.8 vs 5.5 ± 1.7 pmol/g wet weight, P < 0.01), kidney (11.5 ± 1.4 vs 6.5 ± 1.4 pmol/g wet weight, P < 0.01) and pituitary (8.8 ± 2.7 vs 4.8 ± 0.5 pmol/g wet weight, P < 0.01) was higher than in controls, mainly as a result of an increased local production of T₃ from T₄, but plasma-derived T₃ was also higher in most organs. We found an increased intracellular T₃ concentration in the pituitary which may be responsible for the lower plasma TSH concentration in the GH-treated rats. Since the increase in locally produced T₃ is found particularly in liver, kidney and pituitary, typical organs that express 5,-deiodinase activity, we suggest that GH acts on thyroid hormone metabolism by stimulating type-I deiodinase activity.