Abstract
In vitro responsiveness to thyrotropin (TSH) was studied in two surgically excised autonomous hyperfunctioning thyroid nodules; in each instance, the nodules were so characterized in vivo on the basis of baseline 131I uptake and scintiscan and the response therein to exogenous TSH and 1-triiodothyronine administration. Although basal cyclic 3′,5′-adenosine monophosphate (cyclic AMP) levels and 1-14C-glucose oxidation in the nodules did not differ from that in adjacent normal tissue, TSH-induced cyclic AMP formation and glucose oxidation was 2–4-fold greater in the presumably “autonomous” nodules than in normal thyroid. These findings suggest that hyperresponsivity to TSH may play a role in the genesis of autonomous hyperfunctioning thyroid nodules.

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