GROWTH-HORMONE ADMINISTRATION STIMULATES ENERGY-EXPENDITURE AND EXTRATHYROIDAL CONVERSION OF THYROXINE TO TRIIODOTHYRONINE IN A DOSE-DEPENDENT MANNER AND SUPPRESSES CIRCADIAN THYROTROPIN LEVELS - STUDIES IN GH-DEFICIENT ADULTS

OBJECTIVE The impact of exogenous GH on thyroid function remains contr oversial although most data add support to a stimulation of peripheral T4 to T3 conversion. For further elucidation we evaluated iodothyroni ne and circadian TSH levels in GH-deficient patients as part of a GH d ose-response study. PATIENTS Eight GH-deficient adults, who received s table T4 substitution due to central hypothyroidism; two patients, who were euthyroid without T4 supplementation were studied separately. DE SIGN All patients were initially studied after at least 4 weeks withou t GH followed by 3 consecutive 4-week periods in fixed order during wh ich they received daily doses of 1, 2 and 4 IU of GH/m(2) body surface area. The patients were hospitalized for 24 hours at the end of each period. MEASUREMENTS Circulating total and free concentrations of T4 a nd T3, total rT3 and TSH were measured once at the end of each study p eriod. Circadian TSH levels were recorded during the period without GH and during GH treatment with 2 in GH. RESULTS Highly significant GH d ose-dependent increases in total and free T3 and a reduction in rT3 we re observed. The T3/T4 ratio also increased with increasing GH dosages (P < 0.001). In seven patients subnormal T3 levels were recorded in t he period off GH, despite T4 levels well within the normal range. Rest ing energy expenditure also increased and correlated with free T3 leve ls (r = 0.47, P < 0.05). The circadian TSH levels exhibited a signific ant nocturnal increase during the period without GH, whereas GH therap y significantly suppressed the TSH levels and blunted the circadian rh ythm (mean TSH levels (mU/l) 0.546 +/- 0.246 (no GH) vs 0.066 +/- 0.03 1 (2 IU GH) (P < 0.05)). The two euthyroid non-T4 substituted patients exhibited qualitatively similar changes in all parameters. CONCLUSION S GH administration stimulated peripheral T4 to T3 conversion in a dos e-dependent manner. Serum T3 levels were subnormal despite T4 substitu tion when the patients were off GH but normalized with GH therapy. Ene rgy expenditure increased with GH and correlated with free T3 levels. GH caused a significant blunting of serum TSH. These findings suggest that GH plays a distinct role in the physiological regulation of thyro id function in general, and of peripheral T4 metabolism in particular.